There was no evolutionary pressure for it to moderate its virulence.
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I stood next to him so he could feel my virulence.
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He was puzzled by the intensity and the virulence of the opposition.
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Beyond agency, popular usage also includes time, virulence and rapidity of spread.
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At least some of those mutations might be linked to the virulence of Y. pestis.
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And this particular bias has infected contemporary political analysis with a virulence that rivals Ebola.
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It's now commonly acknowledged that the vicious partisanship dividing Washington today has reached unprecedented virulence.
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Given the extreme virulence of those diseases, the apparent rarity of cross-species transmission seemed fortunate.
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Two things explain the virulence with which Brussels and the other euro-zone states have reacted.
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In those circumstances, Dr Ewald argues, the pressure on the virus to reduce its virulence was relieved.
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Excluding that discussion may be contributing to the virulence of the battle against science, including environmental science.
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This year's flu season caught many experts off guard with both its sustained prevalence and its virulence.
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As North Korea has accelerated its weapons programs, it has also ratcheted the virulence of its propaganda.
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Their study, "The evolution of sex-specific virulence in infectious diseases," uses mathematical models to explore this theory.
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But Daley proposes that this particular strain of manipulation is unprecedented in its sophistication, its permanence and its virulence.
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Roy Moore's supporters have distinguished themselves with the virulence with which they refuse to consider the evidence against him.
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If it wasn't created out of the virulence of recent history, it certainly fits perfectly in the current landscape.
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If a pathogen's purpose is to reproduce, it has to balance its virulence with its ability to infect host cells.
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But in his zealousness to rid Old Dominion of white supremacism's virulence, he should be more mindful of the Constitution.
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Despite its virulence, malaria is a treatable, preventable disease – if you have timely access to lifesaving drugs and bed-nets.
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Three aspects of our historical moment are contributing to the virulence of the wave of attacks on Jews and Judaism.
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Because of his leadership, the world may have missed a critical window to halt the pandemic or mitigate its virulence.
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These 30 mutations were located in the genes nrdE, fadJ and pcp—what the team referred to as virulence genes.
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Social media executives get dragged before Congress, apologize for privacy lapses, political manipulation and virulence, and promise to do better.
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The virulence of highly pathogenic bird flu viruses has prompted countries to bar poultry imports from infected countries in earlier outbreaks.
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"Because women can transmit pathogens during pregnancy, birth, or breast-feeding, pathogens adapt, evolving lower virulence in women," the study reads.
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Singh's team expanded beyond that research by evaluating the genetic virulence of the strains and their potential to infect the astronauts.
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Unless you have experienced it, it's difficult to describe the virulence of the Twitter storms that were unleashed on Trump skeptics.
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But health experts now believe that reflected the collapse of the local health system, not just the virulence of the disease.
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The acronym had a double meaning: "W" is the name for a crucial parameter that measures the virulence of dark energy.
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Americans exhausted by Donald Trump's meanspirited virulence will be unlikely to extend confidence to those who continue to play his game.
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While it appears to be transmitted to humans via animals, limiting its virulence, the Chinese government has not disclosed many details.
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The virulence of highly pathogenic bird flu viruses has prompted countries such as Saudi Arabia to bar poultry imports from Bulgaria.
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As if we needed another reminder, the Poway shooting should serve as a warning of the reality and virulence of anti-Semitism.
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But the Trump campaign has made accusations of news media bias a pervasive theme, and has attacked publications and reporters with virulence.
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We are also now living with a long feared "nightmare" scenario in which bacteria gain both increased virulence and resistance to antibiotics.
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Ms Spinney ties the virulence of Spanish flu to its genetic irregularities and does a good job of explaining containment strategies through epidemiology.
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The virulence of the government campaign against supposed external enemies will probably abate a little once Mr Orban has secured a new majority.
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Singh and his colleagues wanted to assess the virulence of the Enterobacter strains on the ISS compared to antimicrobial-resistant pathogens on Earth.
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That may well be the case during the tenure of President Trump: an eruption of sexism and an inability to deny its virulence.
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Stewart's death illuminated for many of them, as if by a flash of lightning, the persistent virulence of racism in the wider society.
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"Now we can look at evolution of specific pathogens, like EBV, and how these bugs change in terms of their virulence," Schroeder said.
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The same year they formed, they released the Ruined EP, seven songs of pure virulence that served as their update on West Coast powerviolence.
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It is hard to predict how changes in the climate and the atmosphere's chemistry will affect the prevalence and virulence of agricultural diseases (see article).
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"It may be possible to switch on the phenotype for women's virulence in pathogens infecting men, thus reducing the mortality they induce," the researchers write.
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First, we need to know how much of a shift this new pathogen is from previous coronavirus strains, based on its infective potential and virulence.
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Undoubtedly, the ongoing effects of the 2008 financial crisis (especially on employment), combined with increasing virulence of Islamist movements such as ISIS, is fueling this growth.
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Now, a team of researchers think that the introduction of a now common sugar additive into our diets, called trehalose, may be responsible for the increased virulence.
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"We argue that breastfeeding, being more prolonged in Japan than in the Caribbean, may have driven the difference in virulence between the two populations," the study reads.
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And while that opposition partly reflects self-interest, Wall Street's Warren hatred has a level of virulence, sometimes crossing into hysteria, that goes beyond normal political calculation.
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Pointing to "infantile heads of state" who speak only "to those who obey, or in order to force obedience," she warned of the virulence of the demagogue.
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Fame-lust itself is a maddening virulence, a deranged will to omnipresence and overexposure that precedes any specific gift or talent, and can exist in their absence.
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The basic case for social distancing is that even small reductions in the virulence of an epidemic can lead to huge reductions in the ultimate death toll.
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For the left in Israel, the virulence of the rightist campaigns reflect an increasingly hostile environment in which liberal values and free speech appear to be under attack.
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The ISS strains had a lot in common with the Earth strains, including genes associated with antimicrobial resistance and virulence (the potential for a microbe to infect a person).
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His mother, Mamie Till, insisted on an open casket in their hometown of Chicago so the world could see what the virulence of racism had done to her son.
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Spinney told me in a phone call that one theory tries to explain the unusual virulence of the 1918 flu by positing that it developed first in Europe's trenches.
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The depth and virulence of racism is brought home to her when her African-American husband gets beaten up so badly she can hardly recognize him in the hospital.
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Some of the virulence directed at him Saturday could perhaps be explained by these positions, though analysts said there was no doubt that anti-Semitism also played a role.
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Photo: GettyTwitter, a social network known for its perpetual feed of virulence and targeted harassment, is turning to academia to answer the decade-old question: Why is it so bad?
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Meanwhile, the country's aging intelligentsia continues to fetishize the intellectuals of the interwar years without scrutinizing their support for the Legionary movement and the inexcusable virulence of their anti-Semitism.
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"Immunosuppression, bacterial virulence and therefore infection risk increase with duration of spaceflight," said senior study author Elisabeth Grohmann, a microbiologist at the Beuth University of Applied Sciences Berlin, in a statement.
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Its blasphemy and anti-Ahmadiyya laws are indefensible, and, through acts of commission and omission, the government deserves blame for the virulence and violence against the Ahmadiyya community throughout Pakistani society.
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This provides the ability to understand how and potentially where a pathogen was prepared, its virulence and physical characteristics and even what medical countermeasures and decontamination techniques might be the most effective.
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It is an insult to the pernicious virulence and exceptional odiousness of McCarthyism for Mr. Dershowitz, the lawyer and professor emeritus at Harvard Law School, to compare his mild experience to it.
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This is not to diminish the virulence of sexism and racism but to honor black men and women who through sheer force of will were able to preserve meaningful lives beyond it.
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Tools like CRISPR could potentially be used to destroy a nation's food supply, to interfere with a person's biology, or to boost the virulence of a virus so that it might better spread.
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And if we are honest, we will agree that the national and international damage done by Mr. Trump's recent white-racist virulence is a heavy moral price to pay, a profound moral tragedy.
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"When we think about a microbe and how bad it is, we think about two things: How easily it spreads, and how nasty it is, its virulence," said Tom Frieden, a former CDC director.
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In evolutionary terms, the optimal strategy for a virus transmitted directly between people, such as the flu, is to moderate its virulence, thereby keeping its host alive long enough to infect as many new hosts as possible.
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In that vein, America doesn't need a referendum on Trump; it needs one on racism and hatred and a political party that's willing to line up as apologists for such virulence in order to win an election.
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But among people who do have acne, P. acnes has higher levels of genes associated with virulence; this strain may be more likely to produce and transport bacterial toxins that can harm the skin and cause inflammation.
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It's a sustained blast of virulence that's grueling to sit through, but Sebastián Lelio's film isn't about intolerance — it is about Marina, played by first-timer Daniela Vega with the presence and infinite watchability of a classical Hollywood star.
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Instead, it suggests the virulence of the classic American malaise: loneliness, the toxic by-product of freedom which generates ad-hoc, fragile communities among people who have escaped conventional backgrounds and who, after dreaming of cosmopolis, wake up atomized.
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When such cases arise and the population is under-immunised (meaning that there are many susceptible children in it) then the vaccine-derived virus can circulate and, over the course of a year or so, reacquire virulence though additional mutations.
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Given the virulence and hostility of the campaign toward certain ethnic and racial groups, it is possible that minority families in particular, such as Latino and African-American families, will be especially suspicious of Trump's motives as commander in chief.
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Underscoring the virulence of the contagion, the national federation of doctors, surgeons and orthodontists said on Friday that 46 colleagues had so far died, six more than a day ago - many of them general practitioners in northern towns and cities.
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His letters to Daisy — and her diary entries — portray someone quite different: a man tired and weary, disheartened by the virulence of his critics, dismayed by the enormousness of the challenges he faced, unsure of his capacities to bear the burdens of office.
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This would seem to be particularly the case considering the record speed with which 35 percent has already been wiped out in U.S. and global equity wealth well as well as the virulence of the global credit crunch that is now underway.
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If, tomorrow, we had a global influenza pandemic akin to the scale and virulence of the one that struck a century ago — in 1918, the Spanish flu killed around 50 million people — it would cost our modern economy an estimated $3 trillion.
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"The one troubling thing about this campaign is the sort of virulence of the anti-Hillary sentiment among some Bernie supporters," he said, noting that he hoped some his posts provided a counterpoint to what Sanders backers might be hearing elsewhere online.
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It was kind of like Microsoft's infamous failed Tay chatbot experiment, except instead of tricking the bot into replying with racist tweets, Jigsaw used the crowdsourced virulence as training data to feed its models, helping to identify and categorize different types of online abuse.
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With respect to its virulence, early genomic sequencing of the Wuhan virus suggests, thankfully, that it is only distantly related to SARS (they are only 73 percent identical), meaning that it is likely to be less deadly, though it is too early to say with confidence.
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"This case, in its details, reinforces the trend in ISIS cases: the preference for weapons other than explosives, the importance of social media, the virulence of ISIS videos, a new trend in efforts to avoid detection online and the youth of these individuals in the United States," she said.
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Sally Hemings has been described as "an enigma," the enslaved woman who first came to public notice at the turn of the 19th century when James Callender, an enemy of the newly elected President Thomas Jefferson, wrote with racist virulence of "SALLY," who lived at Monticello and had borne children by Jefferson.
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"Some parts of the British media do quite frequently refer back to the Second World War as the context of the discussion," Charles Clarke, a former Labour cabinet minister, said at a recent conference, adding that "the virulence" of the way in which some papers seek to set the agenda about Europe has affected the British political debate.
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Three years ago, during the sensational trial of Gilberto Valle, the former New York City police officer who was called the "cannibal cop" by tabloids and charged with conspiracy to kidnap women and illegally retrieve government data, it seemed as if the terrifying online world he inhabited would awaken mainstream interest in the raw virulence directed at women.
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" Yet in that same post, Rhodes directs readers to what he calls "an excellent piece" by Matthew Bracken, which discusses the "persistent virulence of Mohammed's 7th Century plan for global domination" and describes Islam as "a brushfire or ringworm infection: it is dead and barren within the ring, but flares up where it parasitically feeds off the healthy non-Islamic societies around it.
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Any pathogen with a high virulence, high transmission rate and long incubation time may have already caused a catastrophic pandemic before ultimately virulence is limited through natural selection. Additionally, a pathogen that infects humans as a secondary host and primarily infects another species (a zoonosis) has no constraints on its virulence in people, since the accidental secondary infections do not affect its evolution. Lastly, in models where virulence level and rate of transmission are related, high levels of virulence can evolve. Virulence is instead limited by the existence of complex populations of hosts with different susceptibilities to infection, or by some hosts being geographically isolated.
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Strategies to target virulence factors and the genes encoding them have been proposed. Small molecules being investigated for their ability to inhibit virulence factors and virulence factor expression include alkaloids, flavonoids, and peptides. Experimental studies are done to characterize specific bacterial pathogens and to identify their specific virulence factors. Scientists are trying to better understand these virulence factors through identification and analysis to better understand the infectious process in hopes that new diagnostic techniques, specific antimicrobial compounds, and effective vaccines or toxoids may be eventually produced to treat and prevent infection.
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VFDB also known as Virulence Factor Database is a database that provides scientist quick access to virulence factors in bacterial pathogens. It can be navigated and browsed using genus or words. A BLAST tool is provided for search against known virulence factors. VFDB contains a collection of 16 important bacterial pathogens.
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Virulence is a pathogen's or microbe's ability to infect or damage a host. In the context of gene for gene systems, often in plants, virulence refers to a pathogen's ability to infect a resistant host. In most other contexts, especially in animal systems, virulence refers to the degree of damage caused by a microbe to its host. The pathogenicity of an organism - its ability to cause disease - is determined by its virulence factors.
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Virulence is the negative impact that a pathogen (or parasite) has on the Darwinian fitness of a harboring organism (host). For phage, virulence results either in reduction of bacterial division rates or, more typically, in the death (via lysis) of individual bacteria. A number of theory papers exist on this subject, especially as it applies to the evolution of phage latent period. The older phage literature contains numerous references to phage virulence, and phage virulence evolution.
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Expression of virulence genes in E. Carotovora is regulated by N-(3-oxohexanoyl)-l-homoserine lactone (OHHL). Presumably, OHHL-hydrolysis via lactonase reduced OHHL levels, inhibiting the quorom-sensing systems driving virulence gene expression.
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HR can be activated in two main ways: directly and indirectly. Direct binding of the virulence factors to the NLRs can result in the activation of HR. However, this seems to be quite rare. More commonly, the virulence factors target certain cellular proteins that they modify and this modification is then be sensed by NLRs. Indirect recognition seems to be more common as multiple virulence factors can modify the same cellular protein with the same modifications thus allowing one receptor to recognize multiple virulence factors.
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Members of the Clostridium species exhibit a plethora of virulence factors. Common virulence factors associated with gas gangrene include alpha toxin and theta toxin. Clostridium perfingens causes 80–90% of infections and produces both these toxins. ; Alpha toxin (α-toxin) Clostridium perfingens alpha toxin is widely associated with gas gangrene as it is its main virulence factor whilst invading its host.
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Listeriolysin O (LLO) is a hemolysin produced by the bacterium Listeria monocytogenes, the pathogen responsible for causing listeriosis. The toxin may be considered a virulence factor, since it is crucial for the virulence of L. monocytogenes.
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Many different types of virulence factors exist within pathogens, including: adherence factors, invasion factors, capsules, siderophores, endotoxins, and exotoxins. All of these virulence factors either aid directly in host colonization or in host cell and tissue damage.
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Guentzel MN, Berry LJ. Motility as a virulence factor for Vibrio cholerae.
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However, the mechanism by which these proteins contribute to virulence remains unknown.
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There are three general experimental ways for the virulence factors to be identified: biochemically, immunologically, and genetically. For the most part, the genetic approach is the most extensive way in identifying the bacterial virulence factors. Bacterial DNA can be altered from pathogenic to non-pathogenic, random mutations may be introduced to their genome, specific genes encoding for membrane or secretory products may be identified and mutated, and genes that regulate virulence genes maybe identified. Experiments involving Yersinia pseudotuberculosis have been used to change the virulence phenotype of non-pathogenic bacteria to pathogenic.
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Viral genetics encoding viral factors will determine the degree of viral pathogenesis. This can be measured as virulence, which can be used to compare the quantitative degree of pathology between related viruses. In other words, different virus strains possessing different virus factors can lead to different degrees of virulence, which in turn can be exploited to study the differences in pathogenesis of viral variants with different virulence. Virus factors are largely influenced by viral genetics, which is the virulence determinant of structural or non-structural proteins and non-coding sequences.
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As mentioned previously, Pseudomonas aeruginosa produces a host of virulence factors in concert, under the control of the quorum sensing system. Many studies show that inhibiting quorum sensing down-regulates the pathogenicity of Pseudomonas aeruginosa. However, it has been shown that rhamnolipids specifically are a key virulence determinant in Pseudomonas aeruginosa. A variety of virulence factors were analysed in Pseudomonas aeruginosa strains isolated from pneumonia patients.
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The cytolytic peptide Candidalysin is produced during hyphal formation by Candida albicans; it is an example of a virulence factor from a fungus. Other virulence factors include factors required for biofilm formation (e.g. sortases) and integrins (e.g. beta-1 and 3).
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The variable region of the virulence plasmid contain genes that are highly expressed following phagocytosis of R. equi by macrophages. This variable region is believed to be a pathogenicity island that contains genes essential for virulence. A hallmark of the pathogenicity island (PAI) is that many genes within it do not have homologues in other species. The most notable of these are the virulence- associated protein (vap) genes.
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Shiga toxins (Stx) are the primary virulence factors in enterohaemorrhagic E. coli but EHEC produces several other virulence factors capable of damaging the vascular endothelium in EHEC infections. EHEC- Hly is expressed in numerous EHEC serogroups known to cause severe infections in humans. EHEC-Hly is transported within EHEC-secreted outer membrane vesicles (OMVs) in vitro. This mode of transport increases virulence by aiding in EHEC-Hly delivery to target cells.
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The pathogenetic pathways of Streptococcus dysgalactiae have not been explored in detail. Several virulence factors have been identified, but predominantly by screening S. dysgalactiae isolates for homologues of well- characterized S. pyogenes virulence genes. In a study of 216 S. pyogenes virulence genes, S. dysgalactiae was found to harbour approximately half of them. Indeed, whole-genome comparisons reveal a 70% -genetic similarity between the two species, indicating a common genetic ancestry.
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Because of horizontal gene transfer, it is possible to transfer the a clone of the DNA from Yersinia to a non-pathogenic E. coli and have them express the pathogenic virulence factor. Transposon, a DNA element inserted at random, mutagenesis of bacteria DNA is also a highly used experimental technique done by scientists. These transposons carry a marker that can be identified within the DNA. When placed at random, the transposon may be placed next to a virulence factor or placed in the middle of a virulence factor gene, which stops the expression of the virulence factor.
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Among its virulence factors are its capsule, endotoxins, sidenophores, antimicrobial resistance and antigenic phase variation.
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For instance, due to the metal- rich fluids characterizing this areas, a total of 17 genes related with transports systems and detoxification mechanisms of heavy metals (including As, Cd and Cu) were described. Despite this not being a pathogenic bacterium, it possess some virulence genes (including virulence factor mviN, hemolysin or N-linked glycosylation gene cluster) which provide insights into the origins of virulence in their pathogenic relatives, Helicobacter and Campylobacter species.
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A number of studies found that the unfolded protein response contributes to virulence of A. fumigatus.
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However deficiency of DSB repair does not appear to impair M. tuberculosis virulence in animal models.
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The main difference between the serotypes is the expression of Apx toxins and other virulence factors.
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Intimin is a virulence factor (adhesin) of EPEC (e.g. E. coli O127:H6) and EHEC (e.g. E. coli O157:H7) E. coli strains. It is an attaching and effacing (A/E) protein, which with other virulence factors is necessary and responsible for enteropathogenic and enterohaemorrhagic diarrhoea.
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The twin-arginine translocation pathway is an important pathway involved in virulence, which transports proteins through the cell membrane of the bacteria. Over 100 different proteins are thought to be transported by the pathway, some of which are required for virulence, but others just for normal growth.
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The virulence factors implicated in E. rostratum pathogenicity are not well established. E. rostratum is a melanized fungus capable of thriving at mammalian temperatures. In other pathogenic fungi, melanin is a well established virulence factor thought to contribute to virulence by protecting the organism against the immune system of the host. Melanin production has also been associated with drug resistance to polyenes and echinocandins but not to azoles, which is why voriconanole is effective at treating fungal infections.
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The RNA-binding protein Slr1 plays a role in instigating hyphal formation and virulence in C. albicans.
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Cord factor increases the virulence of tuberculosis in mice, but it has minimal effect on other infections.
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The encapsulated, Gram-positive, coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence, prevalence, and extent of drug resistance.
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Many strains have been isolated from the haemolymph of Drosophila melanogaster fruit flies. These strains display different levels of virulence. For example Providencia sneebia is highly virulent, and infection always results in fly mortality. Alternatively, P. rettgeri displays an intermediate virulence wherein some individuals survive infection, while others perish.
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This is achieved through reduced expression of specific virulence genes (typically found on pathogenicity islands) that facilitate the infection process. Specifically, proteobiotics inhibit virulence genes involved in toxin production, biofilm formation, cell adhesionTroll, Marie-Luise. “Investigating the Anti-Virulent Activity of Probiotic Bioactives on Clostridium Perfringens.” M.Sc. Thesis.
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In molecular biology, MvirDB is a publicly available database that stores information on toxins, virulence factors and antibiotic resistance genes. Sources that this database uses for DNA and protein information include: Tox- Prot, SCORPION, the PRINTS Virulence Factors, VFDB, TVFac, Islander, ARGO and VIDA. The database provides a BLAST tool that allows the user to query their sequence against all DNA and protein sequences in MvirDB. Information on virulence factors can be obtained from the usage of the provided browser tool.
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Pyoverdine has been reported to be required for virulence in a variety of disease models, including C. elegans and various models of murine infection (e.g., burn models, pneumonia models, etc.). As noted above, pyoverdine contributes in several fashions to general virulence, including regulating the production of itself, exotoxin A (which stalls translation), and the protease PrpL. There is also evidence that, although not essential for its formation, pyoverdine contributes to the production and development of biofilms that are important for virulence.
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Some relatively avirulent viruses in their natural host show increased virulence upon transfer to a new host species. When an emerging virus first invades a new host species, the hosts have little or no immunity against the virus and often suffer high mortality. Over time, a decrease in virulence in the predominant strain can sometimes be observed. A successful pathogen needs to spread to at least one other host, and lower virulence can result in higher transmission rates under some circumstances.
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A major group of virulence factors are bacterial toxins. These are divided into two groups: endotoxins and exotoxins.
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In this relate, filamentation could be not only a virulence, but also a resistance factor in these bacteria.
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The curtain lecture that followed was of unusual virulence, and in the midst of it he fell asleep.
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In particular, serial passage can be quite useful in experiments that seek to change the virulence of a virus or other pathogen. One consequence of this is that serial passage is useful in creating vaccines, since scientists can apply serial passage and create a strain of virus that has low virulence.
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At least 13 pathotypes are known; virulence is governed by at least three single recessive and independent gene pairs.
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Reassortment of the genome within the genus Orthobunyavirus are not uncommon and can lead to an increase in virulence.
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Carboxysomes are present in all cyanobacteria and many other photo- and chemoautotrophic bacteria. Cyanobacteria are globally significant drivers of carbon fixation, and since they require carboxysomes to do so in current atmospheric conditions, the carboxysome is a major component of global carbon dioxide fixation. Several types of BMCs have been implicated in virulence of pathogens, such as Salmonella enterica and Listeria monocytogenes. BMC genes tend to be upregulated under virulence conditions, and mutating them leads to a virulence defect as judged by competition experiments.
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In bacteria, PinT small RNA is a small regulatory RNA (sRNA) that is activated during stress and virulence conditions. sRNAs base-pair with target mRNAs and modulate their stability or translation. The expression of PhoP-activated sRNA called PinT is highly induced during Salmonella enterica infection. PinT temporally controls Salmonella virulence genes.
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Evidence for plasmid-encoded virulence factors in the phytopathogenic bacterium Clavibacter michiganensis subsp. michiganensis NCPPB382. J. Bacteriol. 175:2131-36.
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Moreover, the complement inhibitory activities of factor H, and other complement regulators, are often used by pathogens to increase virulence.
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Viruses are able to initiate infection, disperse throughout the body, and replicate due to specific virulence factors. There are several factors that affect pathogenesis. Some of these factors include virulence characteristics of the virus that is infecting. In order to cause disease, the virus must also overcome several inhibitory effects present in the host.
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As a defense mechanism, the host environment is hostile to invading pathogens. Therefore, infection can be a stressful event for pathogenic bacteria and control of virulence genes may be temporally correlated with the timing of infection by pathogens. Discovery of RpoS- dependent virulence genes in Salmonella is consistent with RpoS as a general regulator of the stress response: the spv gene found on a virulence plasmid in this bacterium is controlled by RpoS and is required for growth in deep lymphoid tissue such as the spleen and liver.
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The identification of the genetic basis for the causative agent of a disease can be an important component of understanding its effects and spread. Location and content of structural genes can elucidate the evolution of virulence, as well as provide necessary information for treatment. Likewise understanding the specific changes in structural gene sequences underlying a gain or loss of virulence aids in understanding the mechanism by which diseases affect their hosts. For example, Yersinia pestis (the bubonic plague) was found to carry several virulence and inflammation-related structural genes on plasmids.
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In nature, cytochalasin B is involved in fungal virulence, food spoilage and the maintenance of the symbiosis between host and symbiont.
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BCC organisms are typically found in water and soil and can survive for prolonged periods in moist environments. They show a relatively poor virulence. Virulence factors include adherence to plastic surfaces (including those of medical devices) and production of several enzymes such as elastase and gelatinase. Also relevant might be their ability to survive attacks from neutrophils.
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The majority of bacterial pathogens exploit specific adhesion to host cells as their main virulence factor. "A large number of bacterial adhesins with individual receptor specificities have been identified." Many bacterial pathogens are able to express an array of different adhesins. Expression of these adhesins at different phases during infection play the most important role in adhesion based virulence.
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The causes of virulence can vary depending on different strains. The PEL22A strain showed that the genes that regulate the bacteriophage CTXΦ, the main cause of virulence in Vibrio cholerae, were present but lack the genes for cholera toxin, ctxA and ctxB. The strain did contain hlyA gene which codes for hemolysin, an endotoxin found in most Vibrio species.
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It is thought that this characteristic may enhance the virulence of this fungus to first instar nymphs by growing so rapidly it can overcome multiple molts that E. decipiens nymphs undergo. The ability of these fungi to develop in high humidity and moderate temperature environments, in addition to their virulence, make them good potential microbial controls for E. decipiens.
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TCS enable bacteria to respond to changing environments. In V. cholerae several TCS have been identified to be important in colonization, biofilm production and virulence. Recently, small RNAs (sRNA) have been identified as targets of V. cholerae TCS. Here, sRNA molecules bind to mRNA to block translation or induce degradation of inhibitors of expression of virulence or colonization genes.
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Because bacteria use the Pho regulon to maintain homeostasis of Pi, it has the added effect of being used to control other genes. Many of the other genes activated or repressed by the Pho regulon cause virulence in bacterial pathogens. Three ways that this regulon effects virulence and pathogenicity are toxin production, biofilm formation, and acid tolerance.
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To facilitate attachment, invasion, and colonization of its host, this bacterium possesses many virulence factors. Superantigens, bacterial adhesions, and the actions of Yops (which are bacterial proteins once thought to be "Yersinia outer membrane proteins") that are encoded on the "[plasmid] for Yersinia virulence" – commonly known as the pYV – cause host pathogenesis and allow the bacteria to live parasitically.
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Ferulic acid is one of the compounds that initiate the vir (virulence) region of Agrobacterium tumefaciens, inducing it to infect plant cells.
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Respiratory strains may be of relatively low or of high virulence. In Europe, syncytial strains have been found to be highly virulent.
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The p19 protein is considered a significant virulence factor and a component of an evolutionary arms race between plants and their pathogens.
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In plants, guard theory is also known as indirect recognition. This is because rather than direct recognition of a virulence factor or pathogen, there is instead recognition of the end result of a process mediated by a virulence factor or pathogen. In these cases, the virulence factor appears to target an accessory protein that is either a target or a structural mimic of the target of that virulence factor, allowing for plant defences to respond to a specific strategy of pathogenesis rather structures that may evolve and change over time at a faster rate than the plant can adapt to. The interaction between pathogen and accessory protein results in some modification of the accessory protein, which allows for recognition by plant NBS-LRR proteins, which monitor for infection.
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Through careful manipulation and planning, the patient was released into Falstaff Island, to allegedly test the virulence and military capabilities of the worm.
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The Red Queen hypothesis shows that the evolutionary arms race between pathogenic bacteria and humans is a constant battle for evolutionary advantages in outcompeting each other. The evolutionary arms race between the rapidly evolving virulence factors of the bacteria and the treatment practices of modern medicine requires evolutionary biologists to understand the mechanisms of resistance in these pathogenic bacteria, especially considering the growing number of infected hospitalized patients. The evolved virulence factors pose a threat to patients in hospitals, who are immunocompromised from illness or antibiotic treatment. Virulence factors are the characteristics that the evolved bacteria have developed to increase pathogenicity.
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Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors, including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses a plasmin activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate systematic invasion. Many of the bacteria's virulence factors are antiphagocytic in nature. Two important antiphagocytic antigens, named F1 (fraction 1) and V or LcrV, are both important for virulence.
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Many plant pathogens produce virulence factors (i.e., effectors) that modulate or interfere with normal host processes to the benefit of the pathogens. In 2009, a secreted protein, termed “tengu-su inducer” (TENGU; ), was identified from a phytoplasma causing yellowing of onions; this was the first phytoplasmal virulence factor to be described. TENGU induces characteristic symptoms (termed “tengu-su”), including witches’ broom and dwarfism.
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As other virulent bacteria, GBS harbors an important number of virulence factors (virulence factors are molecules produced by bacteria that boosts their capacity to infect and damage human tissues), the most important being the capsular polysaccharide (rich in sialic acid) and a pore-forming toxin, β-hemolysin. Today it is considered that GBS pigment and hemolysin are identical or closely related molecules.
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MeSH - Medical Subject Headings, Karolinska Institute, 13 April 2010 The noun virulence derives from the adjective virulent. Virulent can describe either disease severity or a pathogen's infectivity.Compact Oxford English Dictionary virulent The word virulent derives from the Latin word virulentus, meaning "a poisoned wound" or "full of poison."A Latin Dictionary virulentus In ecology, virulence is the host's parasite-induced loss of fitness.
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Bacterial ABC transporters are essential in cell viability, virulence, and pathogenicity. Iron ABC uptake systems, for example, are important effectors of virulence. Pathogens use siderophores, such as Enterobactin, to scavenge iron that is in complex with high-affinity iron-binding proteins or erythrocytes. These are high-affinity iron-chelating molecules that are secreted by bacteria and reabsorb iron into iron-siderophore complexes.
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The L segment encodes the L endonuclease (an RNA-dependent RNA polymerase enzyme) for genome replication and mRNA synthesis. The M segment encodes a polyprotein, further cleaved in the Gn and Gc surface glycoproteins for attachment and the NSm nonstructural protein that influences virulence. The S segment encodes the NSs protein for immune suppression and virulence, and the N structural nucleocapsid protein.
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The erratic phylogenetic distribution of pathogenic organisms implies that bacterial virulence is a consequence of the presence, or obtainment of, genes that are missing in avirulent forms. Evidence of this includes the discovery of large 'virulence' plasmids in pathogenic Shigella and Yersinia, as well as the ability to bestow pathogenic properties onto E. coli via experimental exposure to genes from other species.
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By doing so, scientists can make a library of the genes using these markers and easily find the genes that cause the virulence factor.
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Some of his ideas on the transmission and virulence of tuberculosis are revolutionary. He died in 1929 and was buried in Montjuïc Cemetery, Barcelona.
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Variation in virulence of the virus has been observed in isolates from Central Africa where strains are more virulent than those from Western Africa.
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Furthermore, increased cytosolic acidity enhances the maturation of SpeB zymogen (SpeBz) into mature SpeB protease (SpeBm) to dramatically increase its proteolytic activity and virulence.
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One or more, and in some cases all five, nematode replicate lines showed declines in virulence, reproduction, heat tolerance, host seeking ability, and nictation.
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Pathogenic strains of E. dermatitidis contain five times more melanin than saprophytic E. dermatitidis, while melanin deficient mutants of pathogenic strains have dramatically reduced virulence.
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The specificity of Mallein tests and the efficiency and potency of it are connected to the "molecular weight of protein fractions, antigenic range, and virulence".
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Adenylate cyclase toxin is a virulence factor produced by some members of the genus Bordetella. Together with the pertussis toxin it is the most important virulence factor of the causative agent of whooping cough, Bordetella pertussis. Bordetella bronchiseptica and Bordetella parapertussis, also able to cause pertussis-like symptoms, also produce adenylate cyclase toxin. It is a toxin secreted by the bacteria to influence the host immune system.
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In contrast, targeted mutation of sidA, the first gene in the siderophore biosynthesis pathway, proved siderophore-mediated iron uptake to be essential for virulence. Mutation of the downstream siderophore biosynthesis genes sidC, sidD, sidF and sidG resulted in strains of A. fumigatus with similar decreases in virulence. These mechanisms of iron uptake appear to work in parallel and both are upregulated in response to iron starvation.
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Listeria uses the cellular machinery to move around inside the host cell. It induces directed polymerization of actin by the ActA transmembrane protein, thus pushing the bacterial cell around. L. monocytogenes, for example, encodes virulence genes that are thermoregulated. The expression of virulence factor is optimal at 39 °C, and is controlled by a transcriptional activator, PrfA, whose expression is thermoregulated by the PrfA thermoregulator UTR element.
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The function of this protein is to facilitate the infection of the host organism. It is a virulence factor designed to induce pathogenesis. One of the major virulence exotoxins is the toxic shock syndrome toxin (TSST), which is secreted by the organism upon successful invasion. It causes a major inflammatory response in the host via superantigenic properties, and is the causative agent of toxic shock syndrome.
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Faine was born in Wellington, New Zealand, 17 August 1926. He graduated BMedSci in 1946 and MB ChB in 1949 from University of Otago. He obtained his DPhil from University of Oxford in 1955 on the virulence of Leptospira icterohaemorrhagiae. He received his MD on virulence in Leptospira from the University of Otago Medical School in 1958 in the Microbiology Unit with Dr. Leopold Kirschner.
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Pathogenicity is the potential disease-causing capacity of pathogens. Pathogenicity is related to virulence in meaning, but some authorities have come to distinguish it as a qualitative term, whereas the latter is quantitative. By this standard, an organism may be said to be pathogenic or non-pathogenic in a particular context, but not "more pathogenic" than another. Such comparisons are described instead in terms of relative virulence.
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This RNA molecule appears to be conserved amongst Listeria species but has not been identified in other bacterial species. It is involved in virulence. The direct mRNA targets of LhrC are the virulence adhesion LapB, and the oligo-peptide binding protein OppA. The 3 conserved UCCC motifs common to all copies of LhrC are involved in the mRNA binding and post-transcriptional repression of the target genes.
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Various virulence factors have been suggested as being involved in the pathogenicity of E. rhusiopathiae. The presence of a hyaluronidase and neuraminidase has been recognized, and neuraminidase was shown to play a significant role in bacterial attachment and subsequent invasion into host cells. The role of hyaluronidase in the disease process is controversial. The presence of a heat-labile capsule has been reported as important in virulence.
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This argument has been disputed on several grounds, including the changing risk due to changing population and behavioral patterns among humans, the limited historical record, and the existence of an anthropic bias. Another argument about the likelihood of pandemics is based on an evolutionary model that predicts that naturally evolving pathogens will ultimately develop an upper limit to their virulence. This is because pathogens with high enough virulence quickly kill their hosts and reduce their chances of spread the infection to new hosts or carriers. This model has limits, however, because the fitness advantage of limited virulence is primarily a function of a limited number of hosts.
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Not all bacteria carry the tatABC genes in their genome;Organism however, of those that do, there seems to be no discrimination between pathogens and nonpathogens. Despite that fact, some pathogenic bacteria such as Pseudomonas aeruginosa, Legionella pneumophila, Yersinia pseudotuberculosis, and E. coli O157:H7 rely on a functioning Tat pathway for full virulence in infection models. In addition, a number of exported virulence factors have been shown to rely on the Tat pathway. One such category of virulence factors are the phospholipase C enzymes, which have been shown to be Tat-exported in Pseudomonas aeruginosa, and thought to be Tat-exported in Mycobacterium tuberculosis.
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The first two would like to activate virulence, but Fusk stops it because the mucous layer, which is a source of fucose, isolates enterocytes from bacteria making the synthesis of the virulence factors useless. However, when fucose concentration decreases because bacterial cells find an unprotected area of the epithelium, then the expression of LEE genes will not be repressed by FusR, and KpdE will strongly activate them. In summary, the combined effect of the QseC/QseF and FusKR provide a fine-tuning system of LEE expression which saves energy and allow the mechanisms of virulence to be expressed only when the chances of success are higher.
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In the spectrum of optimal virulence, vertical transmission tends to evolve benign symbiosis, so is a critical concept for evolutionary medicine. Because a pathogen's ability to pass from mother to child depends significantly on the hosts' ability to reproduce, pathogens' transmissibility tends to be inversely related to their virulence. In other words, as pathogens become more harmful to, and thus decrease the reproduction rate of, their host organism, they are less likely to be passed on to the hosts' offspring, since they will have fewer offspring. Although HIV is sometimes transmitted through perinatal transmission, its virulence can be accounted for because its primary mode of transmission is not vertical.
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Since R. rickettsii needs a moving vector to contract the disease to a viable host it is more likely that this pathogen has moderately low virulence levels. This idea is supported by the tradeoff hypothesis which suggests that virulence of a pathogen will evolve until the level of virulence balances out with the level of transmission to maximize the spread of the pathogen. R. rickettsii invades the endothelial cells that line the blood vessels in the hosts body. Endothelial cells are not phagocytic in nature; however, after attachment to the cell surface, the pathogen causes changes in the host cell cytoskeleton that induces phagocytosis.
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R. rickettsii has evolved a number of strategical mechanisms or virulence factors that allow them to invade the host immune system and successfully infect the host.
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This protein domain, has an important function in forming pili. These are virulence factors crucial for cell adhesion to the host and biofilm formation with successful infection.
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Candidalysin is a cytolytic 31-amino acid α-helical peptide toxin that is released by C. albicans during hyphal formation. It contributes to virulence during mucosal infections.
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Hypovirulence in fungi can be caused by a virus within the fungus. The virus reduces virulence and sporulation. A hypovirus-fungus can be used in biological control.
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These Salmonella-specific functions include many genes for their virulence and characterize the divergence of S. enterica from S. bongori. For instance, the SPI-2 gene which encodes type III secretion systems present in S. enterica is absent in S. bongori. Also, the virulence determinants, specifically effector proteins, are indicated to be more closely related to enteropathogenic E. coli because some of the gene are missing in S. enterica.
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The LasI/LasR and the RhlI/RhlR circuits function in tandem to regulate the expression of a number of virulence genes. At a threshold concentration, LasR binds N-(3-oxododecanoyl)-homoserine lactone. Together this bound complex promotes the expression of virulence factors that are responsible for early stages of the infection process. LasR bound by its autoinducer also activates the expression of the RhlI/RhlR system in P. aeruginosa.
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For example, glucose, mannitol, and fructose reduce antibiotic tolerance in Escherichia coli and Staphylococcus aureus, rendering them more susceptible to killing by aminoglycoside antibiotics. Natural products may be screened for the ability to suppress bacterial virulence factors too. Virulence factors are molecules, cellular structures and regulatory systems that enable bacteria to evade the body’s immune defenses (eg. urease, staphyloxanthin), move towards, attach to, and/or invade human cells (eg.
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Virulence-related outer membrane proteins are expressed in the outer membrane of gram-negative bacteria and are essential to bacterial survival within macrophages and for eukaryotic cell invasion. This family consists of several bacterial and phage Ail/Lom-like proteins. The Yersinia enterocolitica Ail protein is a known virulence factor. Proteins in this family are predicted to consist of eight transmembrane beta-sheets and four cell surface-exposed loops.
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In molecular biology, the domain B, refers to the immunoglobulin-binding domain found in the Staphylococcus aureus virulence factor protein A (SpA). Hence, it is abbreviated to SpAB.
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Basically, there is a trade off between immune function and predatory defense. Thus predation is an import factor when considering the evolution of pathogen virulence and host immunity.
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For viruses to replicate within a host cell and for bacteria to carry out the metabolic processes needed to grow and divide, they must first take in necessary nutrients and transcription factors from their surroundings. Even if a virus is able to bind to a host cell and transfer its genetic material through the cell membrane, the cell may not contain the necessary polymerases and enzymes necessary for viral replication to occur and for pathogenesis to continue. Many pathogens also contain important virulence factors within their genomes. In particular, pathogenic bacteria are capable of translating virulence genes located within their plasmids into different virulence factors in order to aid the bacterium in pathogenesis.
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The ability of bacteria to cause disease is described in terms of the number of infecting bacteria, the route of entry into the body, the effects of host defense mechanisms, and intrinsic characteristics of the bacteria called virulence factors. Many virulence factors are so-called effector proteins that are injected into the host cells by special secretion machines such as the type 3 secretion system. Host-mediated pathogenesis is often important because the host can respond aggressively to infection with the result that host defense mechanisms do damage to host tissues while the infection is being countered. The virulence factors of bacteria are typically proteins or other molecules that are synthesized by enzymes.
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Because of the abundance of so many bacteria that are increasing their resistance to antimicrobial agents such as antibiotics (these products inhibit cell growth or just kill the cell), there is new research coming out about new drugs that reduce virulence factors in some bacteria. Anti-virulent drugs reduce the pathogenic properties in bacteria, allowing the host to attack said bacteria, or allows antimicrobial agents to work. Staphylococcus aureus is a pathogenic bacteria that causes several human infections with a plethora of virulence factors such as: biofilm formation, quorum sensing, and exotoxins to name a few. Researchers took a look at Myricetin (Myr) as a multi-anti-virulence agent against S.areus and how it specifically impacts biofilm formation.
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Target prediction indicated possibility of sRNA interaction with several virulence genes. This study confirmed the presence of one of previously identified Fur regulated sRNAs JA04 identified in strain HK1651.
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Enteropathogenic species of the genus Yersinia bind with the use of the virulence factor YopH to receptors of phagocytes from which they influence the cells capability to exert phagocytosis.
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However, the reader should be warned that virulence is often used as a synonym for "not temperature", a usage which is neither employed here nor to be encouraged generally.
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Labyrinthula have awoken the interest of scientists by being the cause of the "wasting disease" of the seagrass on the North American and European coasts in the 1930s. Since then, several pathogenic species have been identified which mostly live in marine water. Studies testing the virulence of the protist in seagrasses showed a low virulence of Labyrinthula. The protist often lives inside the multicellular organism, but does not initiating any pathogenic event.
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S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocytes) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair the oxidative DNA damages in its genome, caused by this host defense, likely contributes to this pathogen's virulence. Consistent with this premise, Li et al. reported that, among different highly transformable S. pneumoniae isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.
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Mycoplasma penetrans, like many bacteria, exhibits a mechanism by which it can avoid an immune response in the host cells. This avoidance of immune responses is known as a virulence factor. The virulence factor that M. penetrans displays is antigenic variation, the ability to exchange or switch antibodies against which the host cell produces antibodies. The mpl gene encodes for the bacteria's antigens and, like most genes, it contains a promoter region.
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Point mutations in TSV capsid proteins might provide specific isolates with selective advantages such as host adaptability, increased virulence or increased replication ability. Even small variations in the TSV genome can result in substantial differences in virulence. All TSV variants are similar in shape and size, with light variations. The average size of TSV- BZ virus particles is 32.693+/- 1.834 nm compared to TSV-HI with a size of 31.485 +/- 1.187 nm.
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Leptospira noguchii specifically creates a median lethal dose (LD50) of three to 100 leptospires. L. noguchii also uses the Lsa24 protein to avoid the immune system of the host and antibacterials by binding to factor H. While the most important virulence factor has not yet been identified, some of the other proteins that are considered to be contributors to the main virulence are hemolysins, more specifically phospholipase C, sphingomylinase-like proteins, and pore-forming proteins.
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The appearance of cyanobacteria in water storage bodies is becoming of increasing importance and is a major factor in the eutrophication of rivers and streams. Many times the effects of the bacteria's presence can be toxic for livestock and wildlife, as well as for humans. Its exact mode of virulence, however, is still unknown. It has been narrowed down that its virulence is primarily hepatotoxic, although other organs such as the kidneys can be involved.
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Many EAEC encode a transcriptional factor named aggR (aggregative regulator), part of the AraC family of transcription activators. AggR regulates many plasmid, as well chromosomally encoded, virulence factors, that include genes implicated in aggregative adherence fimbriae biogenesis and toxin production. Several toxins have been linked to EAEC virulence, including ShET1 (Shigella enterotoxin 1), Pet (plasmid‐encoded toxin), and EAST-1. However, further studies of these factors have failed to elucidate their role in pathogenesis.
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MLST appears best in population genetic study but it is expensive. Due to the sequence conservation in housekeeping genes, MLST sometimes lacks the discriminatory power to differentiate bacterial strains, which limits its use in epidemiological investigations. To improve the discriminatory power of MLST, a multi- virulence-locus sequence typing (MVLST) approach has been developed using Listeria monocytogenes . MVLST broadens the benefits of MLST but targets virulence genes, which may be more polymorphic than housekeeping genes.
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The degree to which proteobiotics can reduce virulence-gene expression depends on the pathogen and the source of the proteobiotics. Lactobacillus acidophilus-derived proteobiotics down-regulate virulence genes in enterohemorrhagic Escherichia coli, Clostridium difficile, Salmonella Typhimurium, Listeria monocytogenesDelcenserie, V.; Griffiths, M.W. "Mitigation of the Effects of Listeria monocytogenes using probiotics." Presentation at OMAF 2013 Food Safety Research Forum, May 9, 2013, Guelph, ON. and Campylobacter jejuni. Whereas those produced by Bifidobacterium spp.
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As of yet, there have been no negative effects observed within amphibian populations in Madagascar, suggesting that the Bd strain has a low virulence level but should be closely monitored.
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Despite its negligible virulence in humans, it is often tested for in US domestic mosquito control programs as an indicator of fruitful conditions for other mosquito-borne zoonoses to multiply.
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Although Mattern et al. attempted to explore the possibility that these protozoal viruses could function like bacteriophages, they found no significant changes in Entamoeba histolytica virulence when infected by viruses.
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Generally, S100A12 has a significant anti-infectious and antibacterial role that is related to its ability to uptake ions. For example, it inhibits the spread and virulence of H. pylori.
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This type of biofilm formation increases their virulence factor as they are more likely to survive within a host's body, although this type of biofilm is typically associated with capsules.
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Motility is another major virulence factor.Vrancken, K., Holtappels, M., et al. (May 2013). Pathogenicity and infection strategies of the fire blight pathogen Erwinia amylovora in Rosaceae: State of the art.
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Altizer's research interests are ecology of infectious diseases in natural populations, evolution of host resistance and parasite virulence, insect ecology and evolution, animal migrations, and anthropogenic change and infectious disease dynamics.
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Gliding, as a form of motility, appears to allow for interactions between bacteria, pathogenesis, and increased social behaviours. It may play an important role in biofilm formation, bacterial virulence, and chemosensing.
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The disease becomes more distinct when the immediate aquatic environment is poor, and oxygen deficiency increases virulence of the agent. Likewise, excessive ammonium concentration causes an increase in mortality of fish.
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During this time, the vast majority of vertical transmission cases exhibit the initial virulence. In dual inheritance theory, vertical transmission refers to the passing of cultural traits from parents to children.
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This island is around 650,000 base pairs and compromises 75 protein coding genes which includes a type IV secretion system (T4SS) that is responsible for secreting toxins to assist in virulence.
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A greater understanding of how the staphylococci evolve, especially due to the acquisition of mobile genetic elements encoding resistance and virulence genes is helping to identify new outbreak strains and may even prevent their emergence. The widespread incidence of antibiotic resistance across various strains of S. aureus, or across different species of Staphylococcus has been attributed to horizontal gene transfer of genes encoding antibiotic/metal resistance and virulence. A recent study demonstrated the extent of horizontal gene transfer among Staphylococcus to be much greater than previously expected, and encompasses genes with functions beyond antibiotic resistance and virulence, and beyond genes residing within the mobile genetic elements. Various strains of Staphylococcus are available from biological research centres, such as the National Collection of Type Cultures.
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In the early 1940s, Gordon tested thousands of culture plates, trying to find the culture that would have sufficient virulence to make the vaccine. The work was conducted at Western Michigan Laboratories, later known as Kent Community Hospital, located in Grand Rapids, Michigan. Gordon's work focused on pertussis cultures and virulence of the bacterium Bordetella pertussis. Gordon's analysis of pertussis cultures led to identification of a powerful strain of the organism, which enabled the development of an effective vaccine.
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Tribolium castaneum Tribolium castaneum, the red flour beetle, is a host for the microsporidian Nosema whitei. This parasitoid kills its host for transmission, so the host's lifespan is important for the parasite's success. In turn, parasite fitness most likely depends on a trade- off between transmission (spore load) and virulence. A higher virulence would increase the potential for the production of more offspring, but a higher spore load would affect the host's lifespan and therefore the transmission rate.
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The antivirulence strategy needs the knowledge of the pathogenic mechanisms and of the virulence factors that underlie them. Virulence factors are the weapons possessed by pathogens to cause damage to the host, hence they are molecules or bacterial cell structures involved in the various stages of pathogenesis such as adhesion, invasion and colonization and also in the ability to escape host defenses and to injury the host tissues by producing toxic molecules (bacterial endotoxins and exotoxins).
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Alpha-toxin is also one of the key virulence factors in S. aureus pneumonia. The level of alpha-toxin expressed by a particular strain of S. aureus directly correlates with the virulence of the strain. Recent research has shown that immunization with a mutant form of alpha-toxin that is no longer able to form pores protects against S. aureus pneumonia in mice. Also, introduction of alpha-toxin specific antibodies into an unimmunized animal protects against subsequent infection.
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They carry functional genes, such as integrases, transposases, phagocytosis, or part of insertion sequences, to enable insertion into host DNA. PAIs are often associated with tRNA genes, which target sites for this integration event. They can be transferred as a single unit to new bacterial cells, thus conferring virulence to formerly benign strains. PAIs, a type of mobile genetic element, may range from 10-200 kb and encode genes which contribute to the virulence of the respective pathogen.
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When developing vaccines for viruses, the emphasis is on attenuating the virus, or decreasing its virulence, in a given host. Sometimes it is useful to employ serial passage to increase the virulence of a virus. Usually, when serial passage is performed in a species, the result is a virus that is more virulent to that species. For example, one study used serial passage in baboons to create a strain of HIV-2 that is particularly virulent to baboons.
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L. monocytogenes can act as a saprophyte or a pathogen, depending on its environment. When this bacterium is present within a host organism, quorum sensing and other signals cause the up-regulation of several virulence genes. Depending on the location of the bacterium within the host organism, different activators up-regulate the virulence genes. SigB, an alternative sigma factor, up-regulates Vir genes in the intestines, whereas PrfA up-regulates gene expression when the bacterium is present in blood.
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Tir (translocated intimin receptor) is an essential component in the adherence of the enteropathogenic Escherichia coli (EPEC) and enterohemorraghic Escherichia coli (EHEC) to the cells lining the small intestine. To aid attachment, both EPEC and EHEC possess the ability to reorganise the host cell actin cytoskeleton via the secretion of virulence factors. These factors are secreted directly into the cells using a Type three secretion system. One of the virulence factors secreted is the Translocated Intimin Receptor (Tir).
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The PAI can be acquired by horizontal gene transfer and contains genes for several virulence factors. Two fully sequenced variants exist of the V. parahaemolyticus PAI with distinctly different lineages. Each PAI variant contains a genetically-distinct Type III Secretion System (T3SS), which is capable of injecting virulence proteins into host cells to disrupt host cell functions or cause cell death by apoptosis. The two known T3SS variants on V. parahaemolyticus chromosome 2 are known as T3SS2α and T3SS2β.
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In molecular biology, an autotransporter domain is a structural domain found in some bacterial outer membrane proteins. The domain is always located at the C-terminal end of the protein and forms a beta-barrel structure. The barrel is oriented in the membrane such that the N-terminal portion of the protein, termed the passenger domain, is presented on the cell surface. These proteins are typically virulence factors, associated with infection or virulence in pathogenic bacteria.
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Additionally, T4SS also secrete virulence factor proteins directly into host cells as well as taking up DNA from the medium during natural transformation, which shows the versatility of this macromolecular secretion apparatus.
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They can both oxidise arabinose, but only S. liquefaciens can ferment arabinose in peptone water. The virulence of Serratia strains can also be identifiable by type 4 fimbriae, small hair-like projections.
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Legionella has been discovered to be a genetically diverse species with 7-11% of genes strain- specific. The molecular function of some of the proven virulence factors of Legionella have been discovered.
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B. suis is of intermediate virulence and chiefly infects pigs. Symptoms include profuse sweating and joint and muscle pain. Brucellosis has been recognized in animals and humans since the early 20th century.
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Bacteria invest energy into creating these toxins because they act as virulence factors. By targeting immune cells such as macrophages the bacteria will be protected against phagocytosis and destruction by respiratory burst.
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At human body temperature, the thermometer structure opens and to allow transcriptional activator protein ToxT translation, facilitating V. cholerae virulence. Other known RNA thermometers include the ROSE element and Hsp90 cis-reg element.
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Pictures of these symptoms are available at the cited reference. However, latent infections are common. The Clavibacter michiganensis subsp. michiganensis wild type strain NCPPB382 carries two plasmids associated with virulence: pCM1 and pCM2.
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Loney Clinton Gordon (1915–1999) was an African-American chemist and laboratory researcher who assisted doctors Pearl Kendrick and Grace Eldering with bacteriological virulence research leading to the creation of the pertussis vaccine.
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The more it's known about the genomic basis of virulence in historical diseases, the more it can be understood about the emergence and re-emergence of infectious diseases today and in the future.
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Pseudoalteromonas atlantica is a marine bacterium, which has been shown to act as a primary producer of biofilms and exhibit virulence against Cancer pagurus, a species of crab, through secretion of extracellular products.
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Specifically, environmental changes, such as importing birds from a warm to cold environment as well as creating a stressful event for birds in crowded situations, often triggers a virus amplification and increased virulence.
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1977 Feb;15(2):539-48. Eubanks ER, Guentzel MN, Berry LJ. Virulence factors involved in the intraperitoneal infection of adult mice with Vibrio cholerae. Infect Immun. 1976 Feb;13(2):457-63.
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Cysteine proteinases may be another virulence factor because not only do these 30 kDa proteins bind to host cell surfaces but also may degrade extracellular matrix proteins like hemoglobin, fibronectin or collagen IV.
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Hfq protein regulates virB operon which is required for full virulence of the bacteria. It can bind to 5' untranslated region of virB transcriptional regulator BabR and mediate its effects on babR expression.
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Fimbriae are one of the primary mechanisms of virulence for E. coli, Bordetella pertussis, Staphylococcus and Streptococcus bacteria. Their presence greatly enhances the bacteria's ability to attach to the host and cause disease.
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As the complete genome sequences of multiple myxoma strains have been published, scientists have been able to pinpoint exactly which genes are responsible for the changes in the myxoma virus's virulence and behavior.
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All strains isolated from foals and the majority of human, cattle, and pig isolates contain a large plasmid. This plasmid has been shown to be essential for infection of foals, and presumably plays a similar role for infection of other hosts, although this has not been established yet. Strains that lack the virulence plasmid are unable to proliferate in macrophages. This virulence plasmid has been characterised in detail from equine and porcine strains, although only the former has been functionally characterised.
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Infected humans and animals do not transmit their infection to others; they are not infectious. When plated on Niger or birdseed agar, C. neoformans produces melanin, which causes the colonies to have a brown color, and this melanin production is believed to be an important virulence factor.Labrecque O., Sylvestre D. and Messier S. (2005) Systemic Cryptococcus albidus infection in a Doberman Pinscher. J Vet Diagn Invest 17:598-600 C. neoformans produces extracellular vesicles that contain protein components associated with virulence.
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Some disadvantages to the use of bacteriophages also exist, however. Bacteriophages may harbour virulence factors or toxic genes in their genomes and, prior to use, it may be prudent to identify genes with similarity to known virulence factors or toxins by genomic sequencing. In addition, the oral and IV administration of phages for the eradication of bacterial infections poses a much higher safety risk than topical application. Also, there is the additional concern of uncertain immune responses to these large antigenic cocktails.
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It also regulates sRNA in Vibrio cholerae, a specific example being MicX sRNA. In Salmonella typhimurium, Hfq has been shown to be an essential virulence factor as its deletion attenuates the ability of S.typhimurium to invade epithelial cells, secrete virulence factors or survive in cultured macrophages. In Salmonella, Hfq deletion mutants are also non motile and exhibit chronic activation of the sigma mediated envelope stress response. A CLIP-Seq study of Hfq in Salmonella has revealed 640 binding sites across the Salmonella transcriptome.
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The extensive research found about pathogens shows that they can evolve within a month whereas animal hosts such as humans take centuries to make large evolutionary changes. Parasite virulence and host resistance are variables that strongly impact a pathogen’s ability to replicate and be distributed to many hosts. Parasite virulence is the level of harm a host endures due to a virus, bacteria, or parasite. The way a host lives contributes heavily to how their body will react to pathogens.
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Sequencing has revealed a bundle of 12 proteins and some putative hemolysins are potential virulence factors of T. pallidum. 92.9% of DNA was determined to be ORF's, 55% of which had predicted biological functions.
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A number of elastases have been characterized, including those from the serine protease, aspartic protease, and metalloprotease families. Yet, the large redundancy of these elastases has hindered the identification of specific effects on virulence.
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Although the city government was generally held responsible for the virulence of the epidemic, it went largely unchanged. This was the last serious European cholera outbreak, as cities improved their sanitation and water systems.
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In the last step of biofilm formation, the yeast-form cells are released to colonize the surrounding environment (dispersion). Yeast cells released from a biofilm have novel properties, including increased virulence and drug tolerance.
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Asclepias fascicularis is a specific monarch butterfly food and habitat plant. However, it provides around zero cardenolide content, a set of protective chemicals that reduce the virulence of the OE parasite and bird predation.
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Understanding the specific changes in structural genes underlying a gain or loss of virulence is a necessary step in the formation of specific treatments, as well the study of possible medicinal uses of toxins.
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He examined the genetic control of virulence and demonstrated that the virus recombined at high frequency; this observation was not fully appreciated until several years later, when the segmented genome of influenza was demonstrated.
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The knockout of Urease has also proven to decrease virulence capabilities of the fungi. With its wide role in both fungal and bacterial infections, Urease has become an emerging target for current pharmaceutical advancements.
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Consistent with its role as the master controller of the bacterial stress response, RpoS regulates the expression of stress-response genes that fall into various functional categories: stress resistance, cell morphology, metabolism, virulence and lysis.
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In response, thousands of publicly accessible databases and other resources have been created, including the Virulence Factor Database (VFDB) of pathogenic bacteria, which was established in 2004 and was created to aid in pathogenomics research.
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Limiting some microbes' access to iron can reduce their virulence, thereby potentially reducing the severity of infection. Blood transfusion to patients with anemia of chronic disease is associated with a higher mortality, supporting the concept.
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Zot, though absolutely essential for the production of the CTXφ virion, is not actually present in the phage particle. The part that Ace and Zot play in the virulence of cholera is still quite unclear.
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Pseudomonas aeruginosa quorum sensing-dependent virulence factors can be thermoregulated. ROSE thermometer present in the 5'UTR of rhlA and ROSE-like thermometer in the 5'UTR of lasI block the translation at lower temperatures.
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The plcR gene is part of a two-gene operon with papR. The papR gene encodes a small protein which is secreted from the cell and the reimported as a processed heptapeptide forming a quorum-sensing system. The lack of PlcR in B. anthracis is a principle characteristic differentiating it from other members of the B. cereus group. While B. cereus and B. thuringiensis depend on the plcR gene for expression of their virulence factors, B. anthracis relies on the pXO1 and pXO2 plasmids for its virulence.
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The onset was often rapid, and without any precursors that would suggest one was sick. The disease was characterized by an extremely high level of virulence, with death often occurring within a week of one becoming symptomatic. Due to the virulence and effectiveness of the disease, recognizing its existence in the archaeological record has been difficult. Cocoliztli, and other diseases that work rapidly, usually do not leave impacts (lesions) on the deceased’s bones, despite causing significant damage to the gastrointestinal, respiratory, and other bodily systems.
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P. coronata var. avenae uredospores germinate the best at temperature between 10-30 °C with germ-tube growth optimized at 20 °C. The virulence of P. coronata avenae and the resistance of wild oat plants is a highly studied topic. It seems that the resistance level of the oat plant is dependent upon which race of P. coronata avenae is acting on the oat plant; the virulence of the fungal pathogen also seems to depend upon which strain the strain of oat being attacked.
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Mga is a DNA-binding protein that activates the expression of several important virulence genes in Streptococcus pyogenes (group A Streptococcus, GAS) in response to changing environmental conditions. The family also contains VirR like proteins which match only at the C-terminus. Mga is a wide- reaching regulator, affecting gene expression in over 10% of the S. pyrogenes genome. The other large regulator of virulence in GAS is the CovR/S two- component system, which affects the expression of approximately 15% of the genome.
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Guard theory is a branch of immunology which concerns the innate sensing of stereotypical consequences of a virulence factor or pathogen. This is in contrast to the classical understanding of recognition by the innate immune system, which involves recognition of distinct microbial structures- pathogen- associated molecular patterns (PAMPs)- with pattern recognition receptors (PRRs). Some of these stereotypical consequences of virulence factors and pathogens may include altered endosomal trafficking and changes in the cytoskeleton. These recognition mechanisms would work to complement classical pattern recognition mechanisms.
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The various species of Nocardia are pathogenic bacteria with low virulence; therefore clinically significant disease most frequently occurs as an opportunistic infection in those with a weak immune system, such as small children, the elderly, and the immunocompromised (most typically, HIV). Nocardial virulence factors are the enzymes catalase and superoxide dismutase (which inactivate reactive oxygen species that would otherwise prove toxic to the bacteria), as well as a "cord factor" (which interferes with phagocytosis by macrophages by preventing the fusion of the phagosome with the lysosome).
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The most common toxin studied for A. brassicicola is the AB toxin, said to be connected to the virulence, pathogenicity and host range for the fungus. It is most likely produced during conidial germination and probably linked to the ability of the fungus to infect and colonize Brassica leaves However, recent studies have explored new potential metabolites. For example, this fungus also produces histone deacetylase inhibitors, but these do not have a significant impact on lesion size. Some studies show only a 10% reduction in virulence.
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Though, a lot of the hypothetical proteins have role in secondary metabolism, targeting them will be beneficial from two perspectives, i.e., specificity and reducing the virulence of the pathogen with no or minimal undesirable cross-reactivities.
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Comamonas testosteroni is a rare human pathogen associated with acute appendicitis. It is known to have extremely low virulence and very rarely cause disease. Similar to X. azovorans, it was previously classified within the Pseudomonas group.
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Bacterial colonization of intracellular spaces induces the macroscopically visible symptoms including water-soaked lesions on the leaves that later become necrotic.Buttener, Daniela et al. 2003. Genomic Approaches in Xanthomonas campestris pv. Vesicatoria allowing fishing for virulence genes.
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RhbA was found to be transcriptionally upregulated following contact of A. fumigatus with human endothelial cells, and strains with targeted mutation of the rhbA gene showed decreased growth on poor nitrogen sources and reduced virulence in vivo.
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The expression of sRNA-Xcc1 is under the positive control of the two important virulence regulators HrpG and HrpX of Xanthomonas campestris pv. campestris, indicating that sRNA-Xcc1 may be involved in the pathogenesis of the pathogen.
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Another reason appears to be a lessening of the virulence or invasiveness of Streptococcus pyogenes. This organism is also the cause of scarlet fever, which over the same period has also declined markedly in severity and incidence.
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That means that the genes of a virus were integrated into the bacterial genome and made the bacteria pathogenic. The molecular pathway involved in expression of virulence is discussed in the pathology and current research sections below.
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Members of Burkholderia are able to capture and retain foreign DNA. The foreign DNA can be detected by looking for atypical GC context areas. One of the first foreign DNA segments detected this way encoded for virulence.
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E. faecalis is found in most healthy individuals, but can cause endocarditis and sepsis, urinary tract infections (UTIs), meningitis, and other infections in humans. Several virulence factors are thought to contribute to E. faecalis infections. A plasmid-encoded hemolysin, called the cytolysin, is important for pathogenesis in animal models of infection, and the cytolysin in combination with high-level gentamicin resistance is associated with a five-fold increase in risk of death in human bacteremia patients. A plasmid-encoded adhesin called "aggregation substance" is also important for virulence in animal models of infection.
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A prime example concerning the spread of exotoxins is the adaptive evolution of Shiga toxins in E. coli through horizontal gene transfer via transduction with Shigella species of bacteria. Strategies to combat certain bacterial infections by targeting these specific virulence factors and mobile genetic elements have been proposed. For example, horizontally transferred genetic elements play important roles in the virulence of E. coli, Salmonella, Streptococcus and Clostridium perfringens. In prokaryotes, restriction- modification systems are known to provide immunity against horizontal gene transfer and in stabilizing mobile genetic elements.
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In molecular biology, YadA is a protein domain which is short for Yersinia adhesin A. These proteins have strong sequence and structural homology, particularly at their C-terminal end. The function is to promote their pathogenicity and virulence in host cells, though cell adhesion. YadA is found in three pathogenic species of Yersinia, Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica. The YadA domain is encoded for by a virulence plasmid in Yersinia, which encodes a type-III secretion (T3S) system consisting of the Ysc injectisome and the Yop effectors.
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New research on P. atrosepticum virulence pathways has elucidated the use of quorum sensing molecules to exhibit pathogenicity. These pathways include the control of the production of plant cell wall degrading enzymes in addition to other virulence factors. Research indicating the role of other soil microbes in degrading P. atrosepticum quorum sensing communication molecules provides the possibility for safe and effective control of the disease. Plant defense mechanism studies on P. atrosepticum, used to better understand disease resistance, have focused more on the soft-rot symptoms that can sometimes be associated with P. atrosepticum.
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Experimental research, for example, often focuses on creating environments that isolate and identify the role of "niche-specific virulence genes". These are genes that perform specific tasks within specific tissues/places at specific times; the sum total of niche-specific genes is the virus' virulence. Genes characteristic of this concept are those that control latency in some viruses like herpes. Murine gamma herpesvirus 68 (γHV68) and human herpesviruses depend on a subset of genes that allow them to maintain a chronic infection by reactivating when specific environmental conditions are met.
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A useful proxy for virulence is the set-point viral load (SPVL), which is correlated with the time until AIDS. SPVL is the quasi-equilibrium titer of viral particles in the blood during chronic infection. For adaptation towards intermediate virulence to be possible, SPVL needs to be heritable and a trade- off between viral transmissibility and the lifespan of the host needs to exist. SPVL has been shown to be correlated between HIV donor and recipients in transmission pairs, thereby providing evidence that SPVL is at least partly heritable.
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10-kDa culture filtrate protein (CFP-10) is an antigen that contributes to the virulence Mycobacterium tuberculosis. CFP-10 forms a tight 1:1 heterodimeric complex with 6kDaA early secreted antigen target (ESAT-6). In the mycobacterial cell, these two proteins are interdependent on each other for stability. The ESAT-6/CFP-10 complex is secreted by the ESX-1 secretion system, also known as the RD1 region. Mycobacterium tuberculosis uses this ESX-1 secretion system to deliver virulence factors into host macrophage and monocyte white blood cells during infection.
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Likewise, the structural gene responsible for tetanus was determined to be carried on a plasmid as well. Diphtheria is caused by a bacterium, but only after that bacterium has been infected by a bacteriophage carrying the structural genes for the toxin. In Herpes simplex virus, the structural gene sequence responsible for virulence was found in two locations in the genome despite only one location actually producing the viral gene product. This was hypothesized to serve as a potential mechanism for strains to regain virulence if lost through mutation.
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Last accessed June 18, 2007. Transcription of hly, as well as other virulence factors of L. monocytogenes within LIPI-1, is activated by the protein encoded by prfA gene. prfA is thermoregulated by the PrfA thermoregulator UTR element, such that translation of prfA maximally occurs at 37 °C and is nearly silent at 30 °C. Since 37 °C is within the range of normal body temperature, PrfA protein, as well as listeriolysin O and other virulence factors regulated by PrfA, is only produced when L. monocytogenes is in a host.
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When a tag is located, the gene that it disrupts is also thus located (it will reside somewhere between a start and stop codon which mark the boundaries of the gene). STM can be used to discover which genes are critical to a pathogen's virulence by injecting a 'pool' of different random mutants into an animal model (e.g. a mouse infection model) and observing which of the mutants survive and proliferate in the host. Those mutant pathogens that don't survive in the host must have an inactivated gene, required for virulence.
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Pili are responsible for virulence in the pathogenic strains of many bacteria, including E. coli, Vibrio cholerae, and many strains of Streptococcus. This is because the presence of pili greatly enhances bacteria's ability to bind to body tissues, which then increases replication rates and ability to interact with the host organism. If a species of bacteria has multiple strains but only some are pathogenic, it is likely that the pathogenic strains will have pili while the nonpathogenic strains won't. The development of attachment pili may then result in the development of further virulence traits.
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RivX sRNA is a non-coding RNA molecule involved in the interface between two key regulators of virulence in the human pathogen Streptococcus pyogenes (Group A Streptoccus, also known as GAS): the CovR/S system and Mga regulator. This RNA, along with its downstream protein-coding gene RivR, are the first discovered links between these two important regulation networks. An extra protein linking the two pathways, TrxR, was described a year later. The adjoining of these two pathways could allow a consistently high virulence of S. pyogenes despite a variety of environmental conditions.
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In these conditions, some, but not all of the virulence factors associated with the Bvg+ phase are expressed, suggesting this two-component regulatory system can give rise to a continuum of phenotypic states in response to the environment.
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In a study conducted with mice, those that were immunized with autolysin were able to survive longer than the infected mice. This study was able to support as evidence autolysin's contribution in virulence and potential for vaccine antigen.
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As an intercellular signal molecule, indole regulates various aspects of bacterial physiology, including spore formation, plasmid stability, resistance to drugs, biofilm formation, and virulence. A number of indole derivatives have important cellular functions, including neurotransmitters such as serotonin.
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These transfer proteins from the cytoplasm into the periplasm or into the environment around the cell. Many types of secretion systems are known and these structures are often essential for the virulence of pathogens, so are intensively studied.
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Although the process and significance of sequestration were described in detail by two Italian physicians Amico Bignami and Ettore Marchiafava in the early 1890s, it took a century to discover the actual factor for the stickiness and virulence.
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B. burgdorferi is a microaerobic, motile spirochete with seven to 11 bundled perisplasmic flagella set at each end that allow the bacterium to move in low- and high-viscosity media alike, which is related to its high virulence factor.
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HSV-1, upon infecting host cells, induces inflammation and oxidative stress. Thus it appears that the HSV genome may be subjected to oxidative DNA damage during infection, and that MR may enhance viral survival and virulence under these conditions.
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Hypovirus is a genus of viruses, in the family Hypoviridae. Fungi serve as natural hosts. There are currently four species in this genus including the type species _Cryphonectria hypovirus 1_. Diseases associated with this genus include: host virulence reduction.
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Overall, this aids the pathogen in transportation but, also, protection from drugs and sterilizers that would, otherwise, cause death in the pathogen.Cirillo, J., Falkow, S., Tompkins, L., & Bermundez, L. (1997). Interaction of Mycobacterium avium with environmental amoebae enhances virulence.
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SARS usually does not make mice particularly sick, however, after the virus had undergone serial passage in the mice, it had become lethal. Changing the virulence of SARS in this way was important, because without a virulent form of SARS to infect laboratory animals, scientists would have been unable to test the effects of SARS in an animal model. More generally, this experiment also reflects a general medicinal principle: The virulence of a virus is mediated by the difficulty of its transmission. Generally, if a virus kills its host too quickly, the host will not have a chance to come in contact with other hosts and transmit the virus before dying. In serial passage, when a virus was being transmitted from host to host regardless of its virulence, such as Subbaro’s experiment, the viruses that grow the fastest (and are therefore the most virulent) are selected for.
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In 2004, Charpentier published her discovery of an RNA molecule involved in the regulation of virulence-factor synthesis in Streptococcus pyogenes. From 2004 to 2006 she was lab head and an assistant professor at the Department of Microbiology and Immunobiology.
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Cheung GYC, Joo HS, Chatterjee SS, Otto M. Phenol-soluble modulins - critical determinants of staphylococcal virulence. FEMS Microbiology Reviews. Blackwell Publishing Ltd; 2014. pp. 698–719. doi:10.1111/1574-6976.12057 Since their initial discovery, numerous roles of PSMs have been identified.
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Higher levels of protein A in different strains of S. aureus have been associated with nasal carriage of this bacteria. Mutants of S. aureus lacking protein A are more efficiently phagocytosed in vitro, and mutants in infection models have diminished virulence.
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Researchers have conducted many experiments using serial passage. Some of the experimental uses for serial passage include changing the virulence of a virus, to study the evolution or potential evolution of zoonotic diseases to new hosts, and studying antibiotic resistance.
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The characterized PTP-like phytases from ruminal bacteria share sequence and structural homology with the mammalian PTP-like phosphoinositide/-inositol phosphatase PTEN, and significant sequence homology to the PTP domain of a type III-secreted virulence protein from Pseudomonas syringae (HopPtoD2).
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Listeriolysin O is encoded by the gene hly, which is part of a pathogenicity island called LIPI-1.Virulence Factors of Pathogenic Bacteria. "Pathogenicity islands in Listeria: LIPI-1." State Key Laboratory for Molecular Virology and Genetic Engineering, Beijing, China.
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The modified CRISPR-Cas9 system can then be administered to bacterial pathogens using plasmids or bacteriophages. This approach has successfully been used to silence antibiotic resistance and reduce the virulence of enterohemorrhagic E. coli in an in vivo model of infection.
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Finally, although the asd gene encodes an enzyme, aspartate-semialdehyde dehydrogenase, that participates in the synthesis of methionine, lysine and threonine, transcription levels of the asd gene remain constant even when the concentrations of these amino acids are varied. The sRNA was shown to interact with the 5'UTR of the mga transcript (the multiple virulence gene regulator gene) and was renamed MarS for mag- activating regulatory sRNA. In MarS deletion strains expression of mga and several Mga-activated genes is reduced. This down-regulation of virulence factors leads to increased susceptibility of the deletion strain to phagocytosis, reduced adherence to human keratinocytes.
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In molecular biology, LcrV is a protein found in Yersinia pestis and several other bacterial species. It forms part of the Yersinia pestis virulence protein factors that also includes all Yops, or Yersinia outer protein, but the name has been kept out of convention. LcrV's main function is not actually known, but it is essential for the production of other Yops. The type III secretion system of Gram-negative bacteria is used to transport virulence factors from the pathogen directly into the host cell and is only triggered when the bacterium comes into close contact with the host.
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B. cereus is a soil-dwelling bacterium which can colonize the gut of invertebrates as a symbiont and is a frequent cause of food poisoning It produces an emetic toxin, enterotoxins, and other virulence factors. The enterotoxins and virulence factors are encoded on the chromosome, while the emetic toxin is encoded on a 270-kb plasmid, pCER270. B. thuringiensis is an insect pathogen and is characterized by production of parasporal crystals of insecticidal toxins Cry and Cyt. The genes encoding these proteins are commonly located on plasmids which can be lost from the organism, making it indistinguishable from B. cereus.
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Escherichia coli ( Anglicized to ; commonly abbreviated E. coli) is a gram- negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but pathogenic varieties cause serious food poisoning, septic shock, meningitis, or urinary tract infections in humans. Unlike normal flora E. coli, the pathogenic varieties produce toxins and other virulence factors that enable them to reside in parts of the body normally not inhabited by E. coli, and to damage host cells. These pathogenic traits are encoded by virulence genes carried only by the pathogens.
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This indicates that TM7x can suppress the α-TNF gene expression in the macrophages or prevent the detection of its host by macrophages. TM7x is established as an organism that produces toxins and virulence factors, and encodes membrane associated virulence proteins such as OmpA and LemA, type IV secretion systems, and proteins that bind choline. It is also capable of inducing resistance to streptomycin in its host XH001 and thus pose potential threat to humans, as they are involved in various human systemic diseases. including but not limited to vaginal diseases and chronic inflammation in the digestive tract.
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SrbA knockout mutants do not show any signs of in vitro growth in low oxygen, which is thought to be associated with the attenuated virulence. SrbA functionality in hypoxia is dependent upon an upstream cleavage process carried out by the proteins RbdB, SppA, and Dsc A-E. SrbA is cleaved from an endoplasmic reticulum residing 1015 amino acid precursor protein to a 381 amino acid functional form. The loss of any of the above SrbA processing proteins results in a dysfunctional copy of SrbA and a subsequent loss of in vitro growth in hypoxia as well as attenuated virulence.
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Furthermore, Streptococcus dysgalactiae possesses protein G, a virulence factor binding circulating immunoglobulins, and thus interfering with the host antibody response. DrsG, a virulence protein abrogating the effect of antimicrobial peptides secreted by human immune cells, is also harboured by a subset of strains of Streptococcus dysgalactiae subspecies equisimilis. Several toxins and secreted enzymes have been identified in Streptococcus dysgalactiae, including the haemolysins Streptolysin O (SLO) and Streptolysin S (SLS), and a correlation between the expression of SLO and SLS and disease severity has been inferred. speGdys, a homolog of the S. pyogenes superantigen speG, has been documented in some S. dysgalactiae strains.
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Pathogenicity islands carry genes encoding one or more virulence factors, including, but not limited to, adhesins, secretion systems (like type III secretion system), toxins, invasins, modulins, effectors, superantigens, iron uptake systems, o-antigen synthesis, serum resistance, immunoglobulin A proteases, apoptosis, capsule synthesis, and plant tumorigenesis via A. tumefaciens. There are various combinations of regulation involving pathogenicity islands. The first combination is that the pathogenicity island contains the genes to regulate the virulence genes encoded on the PAI. The second combination is that the pathogenicity island contains the genes to regulate genes located outside of the pathogenecity island.
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Over time it was found to have variable virulence in animal models based on which medium it was grown on. Strains with different virulence were then intentionally produced, with H37R being less virulent after growing in acidic media and H37S was more virulent in guinea pigs after being grown in alkaline media (with R standing for resistant to environment, and S for sensitive to environment). The more virulent strain was later renamed H37Rv, with R standing for rough morphology and v standing for virulent. The strain was used for many laboratory studies and became the standard for tuberculosis.
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To fully investigate the role of both toxins in pathogenesis of C. difficile infection, a gene knockout system in a hamster infection model was developed. By permanently knocking out tcdA, tcdB, or both (double knockout), it was shown that C. difficile producing one or both toxins was capable of cytotoxic activity, and this activity translated directly to virulence in vivo. It was also found that a double tcdAtcdB knockout was completely attenuated in virulence. Overall, this research has demonstrated the importance of both TcdA and TcdB in C. difficile infection, showing that either toxin is capable of cytotoxicity.
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This supports their claim that the N-terminus containing the Z-DNA binding residues is necessary for virulence. Overall, these findings show that the similar Z-DNA binding residues within the N-terminus of the E3L protein and the Zα domain are the most important structural factors determining virulence caused by the vaccinia virus, while amino acid residues not involved in Z-DNA binding have little to no effect. A future implication of these findings includes reducing Z-DNA binding of E3L in vaccines containing the vaccinia virus so negative reactions to the virus can be minimized in humans.
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There are most likely multiple traits that control both virulence and resistance which suggests a very interactive host-parasite coevolution. A few specific loci have been found to confer resistance such as Pca which conferred a dominant, resistant phenotype to nine different isolates of P. coronata. An additional isolate of P. coronata was also resisted, although another, un-linked gene may be involved which correlates the theory that resistance and virulence are controlled by A. sativa multiple genes. Some studies suggest that the responses are dependent upon the physiological race of the rust involved due to mutations that arise in separate races.
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Some eukaryotic cells also have cell walls example: fungi (chitin, cell-wall) and Plant cells, but none that are made of peptidoglycan. The outer membrane of gram negative bacteria is rich in lipopolysaccharides, which are combined poly- or oligosaccharide and carbohydrate lipid regions that stimulate the cell's natural immunity. The outer membrane can bleb out into periplasmic protrusions under stress conditions or upon virulence requirements while encountering a host target cell, and thus such blebs may work as virulence organelles. Bacterial cells provide numerous examples of the diverse ways in which prokaryotic cell membranes are adapted with structures that suit the organism's niche.
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On 30 January 1888, Galtier published an article in the Proceedings of the Academy of Sciences.Pierre Galtier, Persistence of rabies virulence in buried corpses (Presented by Mr. Chauveau), Proceedings Academy of Sciences, 1888, Vol 106, pp 364–366. He insisted that "the rabies virus retains its activity in buried corpses, so that when doubts arise afterwards about the nature of the disease that caused the death, exhumation, and inoculation of the bulb are naturally indicated".Pierre Galtier, Persistence of rabid virulence in buried corpses (Presented by Mr. Chauveau), Proceedings of the Academy of Science, 1888, vol 106, p 364.
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Despite the ecological and evolutionary significance of these organisms, many of their biological and pathological features are currently unknown. Through metatranscriptomics using RNA-seq technology combined with field-emission microscopy the virulence factors of a recently described genus of Neobodonida that is considered to be responsible for Ascidian Soft Tunic Syndrome (AsSTS) was revealed.Jang, H.B., Kim, Y. K., Del Castillo, C. S., Nho, S. W., Cha, I. S., and Park, S. B. 2012: RNA-Seq- Based Metatranscriptomic and Microscopic Investigation Reveals Novel Metalloproteases of Neobodo sp. as Potential Virulence Factors for Soft Tunic Syndrome in Halocynthia roretzi.
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Hardships were not lacking in the Mouffetard District. Epidemics of cholera followed one after another. Lack of hygiene and poverty fostered its virulence. Most particularly in 1832 and 1846, the dedication shown and risks taken by Rendu and her Sisters were beyond imagination.
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Bacterial small RNAs play important roles in many cellular processes. RnaG and RyhB sRNAs have been well studied in S. flexneri. Ssr1 sRNA, which could play role in resistance to acidic stress and regulation of virulence was shown to exist only in Shigella.
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Both pathogens rely on a conjugative virulence plasmid to cause disease. In case of R. fascians, this is a linear plasmid, whereas R. equi harbors a circular plasmid. Both pathogens are economically significant. R. fascians is a major pathogen of tobacco plants.
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She currently studies the regulation of biofilm development and virulence in Pseudomonas aeruginosa. Iglewski has published more than 150 research papers and book chapters. She holds seven patents. She has been recognized by the Institute for Scientific Information as a highly cited researcher.
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The ΔlaeA mutant showed increased susceptibility to macrophage phagocytosis and decreased ability to kill neutrophils ex vivo. LaeA regulated toxins, besides gliotoxin, likely have a role in virulence since loss of gliotoxin production alone did not recapitulate the hypo-virulent ∆laeA pathotype.
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However, promotion of proteasomal degradation for the obtention of amino acids may not be the only virulence strategy to obtain carbon and energy sources from the host. Type II–secreted degradative enzymes may provide an additional strategy to generate carbon and energy sources.
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The Ti and Ri plasmids are themselves conjugative. Ti and Ri transfer between bacteria uses an independent system (the tra, or transfer, operon) from that for inter-kingdom transfer (the vir, or virulence, operon). Such transfer creates virulent strains from previously avirulent Agrobacteria.
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Journal of the American Veterinary Medical Association 242:765-767. Success of the disease is determined by the amount and virulence of the bacteria and the resistance of the host.Ganaway, J. R., A. M. Allen, and T. D. Moore. 1971.Tyzzer’s Disease.
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Immune evasion proteins from Staphylococcus aureus have a significant conservation of protein structures and a range of activities that are all directed at the two key elements of host immunity, complement and neutrophils. These secreted virulence factors assist the bacterium in surviving immune response mechanisms.
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Similar studies have investigated the genes responsible for motility in Campylobacter species. All Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence. The number of known quinolone-resistant strains is growing.
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Another factor contributing to antifungal resistance is the presence of a set of genes known to be involved in biofilm formation. More studies are needed to determine whether the phylogenetic divergence of C.auris clones exhibits region-specific patterns of invasiveness, virulence, and/or drug resistance.
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U.S. interest in glanders (agent LA) continued through the 1950s, except it had an inexplicable tendency to lose virulence in the lab, making it difficult to weaponize. Between 1982 and 1984, the Soviet Union allegedly used weaponized B. mallei during the Soviet–Afghan War.
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The complex and unique cell wall that makes members of the genus Mycobacterium difficult to destroy is apparently also the reason for the extremely slow replication rate. Virulence factors include a waxy exterior coating, formed by the production of mycolic acids unique to Mycobacterium.
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Classified activities were moved underground, and several new laboratories have been constructed and equipped to work with highly dangerous pathogens. One of their current subjects is reportedly Bacillus anthracis strain H-4. Its virulence and antibiotic resistance have been dramatically increased using genetic engineering.
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N. gonorrhoeae is host restricted almost entirely to humans. "Extensive studies have established type 4 fimbrial adhesins of N. gonorrhoeae virulence factors." These studies have shown that only strains capable of expressing fimbriae are pathogenic. High survival of polymorphonuclear neutrophils (PMNs) characterizes Neisseria gonorrhoeae infections.
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In biology, similar principles are used in order to classify and define groups of different biological objects, for example, to define phage types of Salmonella enteritidis based on Fourier transform infrared spectra, to detect animal source of Escherichia coli studying its virulence factors etc.
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In epidemics with such superspreader events (SSEV), the majority of individuals infect relatively few secondary contacts. SSEVs are shaped by multiple factors including a decline in herd immunity, nosocomial infections, virulence, viral load, misdiagnosis, airflow dynamics, immune suppression, and co-infection with another pathogen.
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Naiyer S, Kaur D, Ahamad J, Singh SS, Singh YP, Thakur V, Bhattacharya A, Bhattacharya S. Transcriptomic analysis reveals novel downstream regulatory motifs and highly transcribed virulence factor genes of Entamoeba histolytica. BMC Genomics. 2019 Mar 12;20(1):206. doi: 10.1186/s12864-019-5570-z.
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Melaka virus is a nonenveloped, segmented, double-stranded RNA virus. Having a segmented genome facilitates reassortment. Melaka is a fusogenic virus which enhances virulence in its ability to carry out cell-cell fusion.Day JM. The diversity of the orthoreoviruses: molecular taxonomy and phylogenetic divides.
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Recent studies have discovered that anaerobiosis can significantly impact the major regulatory circuit of quorum sensing. This important link between quorum sensing and anaerobiosis has a significant impact on production of virulence factors of this organism.Cornelis P. 2008. Pseudomonas: Genomics and Molecular Biology (1st ed.).
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Represses the translation of the transcriptional regulator MgrA by binding to its mRNA, enhances biofilm formation and decreases bacterial virulence. Other mRNAs: including SsaA-like enzymes involved in peptidoglycan metabolism and the secreted anti-inflammatory FLIPr protein were validated as direct targets of RsaA.
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Xin, X.F. and S.H. He. 2013. Pseudomonas syringae pv. Tomato DC3000: a model pathogen for probing disease susceptibility and hormone signaling in pants. Annu. Rev. Phytopathol. 51:473-498. The ability to target receptor kinases is required for the virulence function of AvrPto in plants.
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LuxS influences iron uptake in pneumococcal species, which also affects biofilm formation. LuxS mutant D39luxS has reduced virulence when compared to wild type studies done on the intranasal channels of mice, and experiments have shown that this mutant also has significantly decreased biofilm formation capabilities.
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The src gene is not essential for RSV proliferation but it greatly increases virulence when present. Src is a tyrosine kinase involved in regulation of cell growth and differentiation. It has an SH2 and SH3 domain, which are responsible for its activation and deactivation.
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On bacterial internalization it controls the expression of invasion associated effectors (SPI-1) through the direct base-pairing with the mRNA. Later in infection it represses the virulence genes (SPI-2) allowing the switch from an invasive state to the state of intracellular replication.
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The capsule is considered a virulence factor because it enhances the ability of bacteria to cause disease (e.g. prevents phagocytosis). The capsule can protect cells from engulfment by eukaryotic cells, such as macrophages. A capsule-specific antibody may be required for phagocytosis to occur.
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Infection and Immunity 63 (9): 3484-3490. C. canimorsus generally has low virulence in healthy individuals,Lion C, Escande F and Burdin JC. 1996. Capnocytophaga canimorsus Infections in Human: Review of the Literature and Cases Report. European Journal of Epidemiology 12 (5): 521-533.
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Chromatin immunoprecipitation studies with the SrbA protein led to the identification of a second hypoxia regulator, SrbB. Although little is known about the processing of SrbB, this transcription factor has also shown to be a key player in virulence and the fungal hypoxia response. Similar to SrbA, a SrbB knockout mutant resulted in a loss of virulence, however, there was no heightened sensitivity towards antifungal drugs nor a complete loss of growth under hypoxic conditions (50% reduction in SrbB rather than 100% reduction in SrbA). In summary, both SrbA and SrbB have shown to be critical in the adaptation of A. fumigatus in the mammalian host.
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The disease in swine became much more severe, outbreaks of respiratory disease in cattle rose dramatically, and the infection was spread airborne to other swine herds. The higher virulence of these virus strains was associated with a certain ability to create syncytia (cell fusion) in tissue cultures (syncytial virus strains). Comprehensive restriction fragment pattern analyses of virus DNA have documented that the more virulent strains had not been introduced from abroad but had developed in two steps from the original Danish strains. The correlation between high virulence of virus strains and syncytium formation in tissue cultures was confirmed by examinations of isolates from other countries.
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A Bacillus cereus cell that has undergone filamentation following antibacterial treatment (upper electron micrograph; top right) and regularly sized cells of untreated B. cereus (lower electron micrograph) Antibiotics can induce a broad range of morphological changes in bacterial cells including spheroplast, protoplast and ovoid cell formation, filamentation (cell elongation), localized swelling, bulge formation, blebbing, branching, bending, and twisting. Some of these changes are accompanied by altered antibiotic susceptibility or altered bacterial virulence. In patients treated with β-lactam antibiotics, for example, filamentous bacteria are commonly found in their clinical specimens. Filamentation is accompanied by both a decrease in antibiotic susceptibility and an increase in bacterial virulence.
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In some bacteria sRNAs regulate virulence genes. In Salmonella, the pathogenicity island encoded InvR RNA represses synthesis of the major outer membrane protein OmpD; another co-activated DapZ sRNA from 3'-UTR represses abundant membrane Opp/Dpp transporters of oligopeptides; and SgrS sRNA regulates the expression of the secreted effector protein SopD. In Staphylococcus aureus, RNAIII regulates a number of genes involved in toxin and enzyme production and cell-surface proteins. The FasX sRNA is the only well-characterized regulatory RNA known to control the regulation of several virulence factors in Streptococcus pyogenes, including both cell-surface associated adhesion proteins as well as secreted factors.
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No single effector protein has been found to significantly alter pathogenicity of R. solanacearum, but simultaneous disruption of certain subsets of effectors (such as the set of seven GALA effectors in strain GMI1000) strongly affects virulence of the pathogen. GALA 7 is necessary for virulence on Medicago truncatula, hinting that T3E diversity may play a role in determining the broad host range of the R. solanacearum species complex. The type III secretion system is not unique to R. solanacearum, and is, in fact, very ancient. The evolutionary history of the T3SS is contested; a high degree of similarity to the flagellum has sparked debate over the relationship between these two structures.
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HR is triggered by the plant when it recognizes a pathogen. The identification of a pathogen typically occurs when a virulence gene product, secreted by a pathogen, binds to, or indirectly interacts with the product of a plant R gene. R genes are highly polymorphic, and many plants produce several different types of R gene products, enabling them to recognize virulence products produced by many different pathogens. In phase one of the HR, the activation of R genes triggers an ion flux, involving an efflux of hydroxide and potassium to the outside the cells, and an influx of calcium and hydrogen ions into the cells.
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Some industrial strains are also capable of growing above 37 °C. European Food Safety Authority (as of 2017) requires that all S. cerevisiae strains capable of growth above 37 °C that are added to the food or feed chain in viable form must, as to be qualified presumably safe, show no resistance to antimycotic drugs used for treatment of yeast infections. The ability to grow at elevated temperatures is an important factor for strain's virulence but not the sole one. Other traits that are usually believed to be associated with virulence are: ability to produce certain enzymes such as proteinase and phospholipase, invasive growth (i.e.
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Virulence (the tendency of a pathogen to reduce a host's fitness) evolves when a pathogen can spread from a diseased host, despite the host becoming debilitated. Horizontal transmission occurs between hosts of the same species, in contrast to vertical transmission, which tends to evolve toward symbiosis (after a period of high morbidity and mortality in the population) by linking the pathogen's evolutionary success to the evolutionary success of the host organism. Evolutionary biology proposes that many pathogens evolve an optimal virulence at which the fitness gained by increased replication rates is balanced by trade-offs in reduced transmission, but the exact mechanisms underlying these relationships remain controversial.
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Clumping factor A, or ClfA, is a virulence factor from Staphylococcus aureus (S. aureus) that binds to fibrinogen. ClfA also has been shown to bind to complement regulator I protein. It is responsible for the clumping of blood plasma observed when adding S. aureus to human plasma.
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Currently, new methods of detecting bacterial toxins are being developed to better isolate and understand these toxins. Potential applications of toxin research include combating microbial virulence, the development of novel anticancer drugs and other medicines, and the use of toxins as tools in neurobiology and cellular biology.
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J. D. Mansi (ed.), Sacrorum Conciliorum nova et amplissima collectio, editio novissima, Tomus decimus nonus (19) (Venice: A. Zatta 1774), pp. 41-42. In 1410 the plague struck Parma with especial virulence. It is claimed that one-quarter of the population died.Allodi, I, pp. 681-682.
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However, Ionescu moved away from the monarchy due to Carol's inner circle. Ionescu's antisemitism was a decisive factor in his switching of allegiances: Jewish writer Mihail Sebastian's Journal depicts the interval during which Ionescu's virulence grew, as well as the reasons that were animating his large following.
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Essentially, the main function of the YadA domain is to help cell adhesion and to increase virulence. YadA is a collagen-binding outer membrane protein. It forms the fibrillar matrix on the bacterial cell surface. This aids cell attachment and helps the bacteria invade eukaryotic cells.
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Some human cases have been successfully treated with trimethoprim/sulfamethoxazole and fluoroquinolones. B. bronchiseptica does not express pertussis toxin, which is one of the characteristic virulence factors of B. pertussis, but it has the genes to do so, highlighting the close evolutionary relationship between the two species.
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Anti- inflammatory therapy can help shorten recovery times, but topical corticosteroids should be used with care if corneal ulcers are present. M. bovis uses several different serotyped fimbriae as virulence factors, consequently pharmaceutical companies have exploited this to create vaccines. However, currently available vaccines are not reliable.
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The advantage of using those autotrophies lies in the fact that they exhibit wild-type or nearly wild-type virulence in a mouse model compared to the URA3 system. One application of the leucine, arginine and histidine autotrophy is for example the candida two-hybrid system.
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According to evolutionary medicine, optimal virulence increases with horizontal transmission (between non-relatives) and decreases with vertical transmission (from parent to child). This is because the fitness of the host is bound to the fitness in vertical transmission but is not so bound in horizontal transmission.
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Diodoros, 4.12.3-8. He died quickly as a result of the poison's outrageous virulence and was found by Heracles. Hyginus (in his De Astronomia) reports versions of the story where it is not Pholus's foot on which the poison arrow accidentally falls, but Chiron's instead.Gantz, p. 392.
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It is a small bacillus that can withstand weak disinfectants and can survive in a dry state for weeks. Its unusual cell wall is rich in lipids such as mycolic acid and is likely responsible for its resistance to desiccation and is a key virulence factor.
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Bunyaviruses and innate immunity. In: Cellular signaling and innate immune responses to RNA virus infections. (2009) Washington, DC: ASM Press. pp. 287–299. This would establish it as the main virulence factor as it acts during the transcriptional phase by inhibiting RNA polymerase II–mediated transcription.
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Metal-ion dependent regulators orchestrate the virulence of several important human pathogens. The dtxR protein regulates the expression of diphtheria toxin in response to environmental iron concentrations. Furthermore, dtxR and ideR control iron uptake. Homeostasis of manganese, which is an essential nutrient, is regulated by mntR.
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The sequestration of antioxidant materials in cells walls may also serve as a virulence factors for this agent. A yeast-like phase has also been reported from the blood of infected individuals. P. obovatum can cause localized or disseminated infections the latter of which are occasionally fatal.
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Xanthomonas axonopodis has the capability to form a biofilm for attachment on the host. The biofilm is the result of the production of extracellular polysaccharides (xanthan). The biofilm ensures the virulence and epiphytic survival of X. axonopodis pv. citri prior to the development of citrus canker.
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Commonly caused by bacterial infection, as in the case of cellulitis or diverticulitis. Non-infectious causes of phlegmon include acute pancreatitis, where inflammation is caused by leaking of pancreatic digestive enzymes into the surrounding tissues. Factors affecting the development of phlegmon are virulence of bacteria and immunity strength.
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Serotypes B:1 and B:3,4 have caused a septicaemic disease in antelope (Antilocapra americana) and elk (Cervus canadensis), respectively. Serotype B:4 was associated with the disease in bison (Bison bison). Rimler RB (1993) Serology and virulence of haemorrhagic septicaemia Pasteurella multocida isolatd from domestic and feral ruminants.
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The speed and transcription inaccuracies of RNA viruses give rise to antigenically distinct varieties in a single host animal. These quasispecies don't necessarily give rise to population-wide new organisms. The rate of proliferation of quasispecies has significant implication for host immune control, and therefore virulence of the organism.
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The Bs2 NLR gene from the wild pepper, Capsicum chacoense, was moved into tomato, where it inhibited pathogen growth. Field trials demonstrated robust resistance without bactericidal chemicals. However, rare strains of Xanthomonas overcame Bs2-mediated resistance in pepper by acquisition of avrBs2 mutations that avoid recognition but retain virulence.
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Collagenases are enzymes that break the peptide bonds in collagen. They assist in destroying extracellular structures in the pathogenesis of bacteria such as Clostridium. They are considered a virulence factor, facilitating the spread of gas gangrene. They normally target the connective tissue in muscle cells and other body organs.
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An attenuated vaccine is a vaccine created by reducing the virulence of a pathogen, but still keeping it viable (or "live"). Attenuation takes an infectious agent and alters it so that it becomes harmless or less virulent. These vaccines contrast to those produced by "killing" the virus (inactivated vaccine).
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These hair like structures are important virulence factors for different pathogenic strains of Bacteria as they can mediate biofilm formation and adhesion to host epithelia. Other examples include Salmonella enterica serovar Typhimurium and Klebsiella pneumoniae. More generally, Lrp facilitates the proliferation and pathogenesis of bacteria in their hosts.
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The virulence of Luther's language however, was off-putting to some. After the publication of this work, with its harsh condemnation of the papacy, the renowned humanist Erasmus, who had previously been cautiously supportive of Luther's activities, became convinced that he should not support Luther's calls for reform.
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Elisa Teresa Granato (born 23 April 1988) is a molecular microbiologist in the Departments of Zoology and Biochemistry at the University of Oxford, where she researches bacterial interactions and how they evolved, including the significance of features of bacteria that contribute to disease, also known as virulence factors.
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A leading Russian newspaper, Novoe Vremia [New Times] started attacking the Jews in the late 1870s. Its virulence increased during the revolutionary years 1904–06, when it charged Jews with seeking to dominate Russia.Daniel Balmuth, "Novoe Vremia’s War Against the Jews." East European Jewish Affairs 35.1 (2005): 33-54.
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Y. pestis is thought to be descended from Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids. A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006. The analysis focused on the transition to a growth condition mimicking growth in host cells.
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Such criteria include whether there is a structure available, conservation of the bacterial gene in the human genome (e.g. domain sharing), availability of computational or experimental evidence of gene function, phenotypical considerations (such as presence in a pathogen or relation to antibiotic resistance, pathogenicity or virulence) and others.
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The allometry between host and parasite body sizes constitutes an evident aspect of host–parasite coevolution. The slope of this relationship is a taxon- specific character. Parasites' body size is known to covary positively with fecundity and thus it likely affects the virulence of parasitic infections as well.
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Similarly, USPs are crucial for the survival of Salmonella, the causative agent in Salmonellosis. In developing countries, food poisoning of this kind is a potentially life- threatening condition. The USPs have influence in growth arrest, stress responses and virulence. UspA is induced by metabolic, oxidative and temperature related stress.
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Low pathogenic avian influenza H5N2 virus in poultry later gained accentuated virulence in the United States Kawaoka Y, Naeve CW, Webster RG (1984). "Is virulence of H5N2 influenza viruses in chickens associated with loss of carbohydrate from the hemagglutinin?". Virology 139: 303-16. and Mexico.Horimoto T, Rivera E, et al (1995). "Origin and molecular changes associated with emergence of a highly pathogenic H5N2 influenza virus in Mexico". Virology 213: 223-30. A highly pathogenic strain of H5N2 caused flu outbreaks with significant spread to numerous farms, resulting in great economic losses in 1983 in Pennsylvania, USA in chickens and turkeys, in 1994 in Mexico in chickens and a minor outbreak in 1997 in Italy in chickens.
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Like all noroviruses, MNV has linear, non-segmented, positive-sense RNA genome of approximately 7.5 kbp, encoding a large polyprotein which is cleaved into six smaller non-structural proteins (NS1/2 to NS7) by the viral 3C-like protease (NS6), a major structural protein (VP1) of about 58~60 kDa and a minor capsid protein (VP2). In addition to these proteins, MNV is unique amongst the noroviruses in possessing an additional fourth open reading frame overlapping the VP1 coding sequence. This additional reading frame encodes a virulence factor (VF1) which regulates the innate immune response. The 3'UTR of the viral genome forms stem-loop structures which have a role in virulence.
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Some mosquito-transmitted rabbit viruses are only transmitted to uninfected rabbits from infected rabbits which are still alive. This creates a selective pressure on every group of viruses already infecting a rabbit not to become too virulent and kill their host rabbit before enough mosquitoes have bitten it, since otherwise all the viruses inside the dead rabbit would rot with it. And indeed in natural systems such viruses display much lower virulence levels than do mutants of the same viruses that in laboratory culture readily outcompete non-virulent variants (or than do tick- transmitted viruses since ticks do bite dead rabbits). In the previous passage, the group is assumed to have "lower virulence", i.e.
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Antivirulence is the concept of blocking virulence factors. In regards to bacteria, the idea is to design agents that block virulence rather than kill bacteria en masse, as the current regime results in much more selective pressure (on antibiotic resistance). From the early 1950s onwards, a large number of antibiotics, due to the emergence of multidrug-resistant common pathogen strains (both gram-negative and gram-positive), became scarcely effective and not-useful. This scenario has stimulated the research for an alternative strategy focused on agents (antivirulence or antipathogenic agents) aimed to disarm microorganisms cause of infectious disease, without killing or inhibiting the growth of microorganisms themselves and therefore with limited selective pressure to promote the antibiotic resistance phenomenon.
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As Z-DNA has been researched more thoroughly, it has been discovered that the structure of Z-DNA can bind to Z-DNA binding proteins through london dispersion and hydrogen bonding. One example of a Z-DNA binding protein is the vaccinia E3L protein, which is a product of the E3L gene and mimics a mammalian protein that binds Z-DNA. Not only does the E3L protein have affinity to Z-DNA, it has also been found to play a role in the level of severity of virulence in mice caused by vaccinia virus, a type of poxvirus. Two critical components to the E3L protein that determine virulence are the N-terminus and the C-terminus.
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PTV is a member of the phlebotomus fever subgroup of Phleboviruses, and as the name suggests, causes an acute febrile illness. Acute febrile illness in humans is characterized by a rapid onset of fever that is often accompanied by secondary symptoms such as a headache, chills, myalgias and arthralgias. This illness will last for about 2–5 days and is not considered to be highly virulent in humans, however, testing in Syrian hamsters has revealed high virulence for the PTV-A serotype and a low virulence for the PTV-B serotype. Although relatively low numbers of human infection with this virus have been reported, the virus is of public health interest and further research will need to be conducted.
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Sequencing data of M. hakonensis also revealed the presence of the gene for Urease, a common virulence factor found in gastro-pathogenic bacteria such as Helicobacter pylori, a common infection causing about 14,500 deaths per year. Urease catalyzes the degradation of urea to ammonia and bicarbonate, increasing the pH of the stomach, which allows for survival and manifestation of the pathogens. Recent studies have revealed that Urease also plays a role in fungal virulence, found in organisms such as C. neoformans and Co. posadasii. Urease causes a shift in immune response from a Type 1 (Th1 cells) immune response to a Type 2 (Th2 cells) immune response, reducing the ability of the host immune response to prevent infection.
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The international biological hazard symbol Ideal characteristics of a biological agent to be used as a weapon against humans are high infectivity, high virulence, non-availability of vaccines and availability of an effective and efficient delivery system. Stability of the weaponized agent (the ability of the agent to retain its infectivity and virulence after a prolonged period of storage) may also be desirable, particularly for military applications, and the ease of creating one is often considered. Control of the spread of the agent may be another desired characteristic. The primary difficulty is not the production of the biological agent, as many biological agents used in weapons can be manufactured relatively quickly, cheaply and easily.
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P. multocida expresses a range of virulence factors including a polysaccharide capsule and the variable carbohydrate surface molecule, lipopolysaccharide (LPS). The capsule has been shown in strains of serogroups A and B to help resist phagocytosis by host immune cells and capsule type A has also been shown to help resist complement-mediated lysis.Chung JY, Wilkie I, Boyce JD, Townsend KM, Frost AJ, Ghoddusi M, Adler B: Role of capsule in the pathogenesis of fowl cholera caused by Pasteurella multocida serogroup A. Infect Immun 2001, 69(4):2487-2492.Boyce JD, Adler B: The capsule is a virulence determinant in the pathogenesis of Pasteurella multocida M1404 (B:2). Infect Immun 2000, 68(6):3463-3468.
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However, this cost may be overwhelmed by the short term benefit of higher infectiousness if transmission is linked to virulence, as it is for instance in the case of cholera (the explosive diarrhea aids the bacterium in finding new hosts) or many respiratory infections (sneezing and coughing create infectious aerosols).
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The list of small RNAs involved in the control of bacterial virulence in S. aureus is growing. This can be facilitated by factors such as increased biofilm formation in the presence of increased levels of such small RNAs. For example, RNAIII, SprD, SprC, RsaE, SprA1, SSR42, ArtR, SprX, and Teg49.
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However, these measures only reduce microbe populations rather than eliminate them. Microgravity may increase the virulence of specific microbes. It is therefore important that the mechanisms responsible for this problem are studied and the appropriate controls are implemented to ensure that astronauts, in particular, those that are immunocompromised, are not affected.
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A virus genus is a group of related species that share some significant properties and often only differ in host range and virulence. A genus name must be a single word ending in the suffix -virus. Approval of a new genus must be accompanied by the approval of a type species.
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The ability to switch between yeast cells and hyphal cells is an important virulence factor. Many proteins play a role in this process. Filamentation in C. albicans is a very complex process. The formation of hyphae can for example help Candida albicans to escape from macrophages in the human body.
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Immunoglobulins are antibodies expressed and secreted by hosts in response to an infection. These immunoglobulins play a major role in destruction of the pathogen through mechanisms such as opsonization. Some bacteria, such as Streptococcus pyogenes, are able to break down the host's immunoglobulins using proteases. Viruses also have notable virulence factors.
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A major group of virulence factors are proteins that can control the activation levels of GTPases. There are two ways in which they act. One is by acting as a GEF or GAP, and proceeding to look like a normally eukaryotic cellular protein. The other is covalently modifying the GTPase itself.
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Pathogenicity islands (PAIs) are gene clusters incorporated in the genome, chromosomally or extrachromosomally, of pathogenic organisms, but are usually absent from those nonpathogenic organisms of the same or closely related species.Kaper JB, Hacker J, eds. 1999. Pathogenicity Islands and Other Mobile Virulence Elements. Washington, DC: Am. Soc. Microbiol. 1-11.
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Infection of macrophages by B. abortus is stimulated by blue light in the wild type, but is limited in photochemically inactive and null mutants, indicating a flavin-containing histidine kinase functions as a photoreceptor regulating B. abortus virulence. Conversely, depriving Brucella of the blue wavelengths dropped its reproductive rate by 90%.
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Rae, R. G., Tourna, M., & Wilson, M. J. (2010). The slug parasitic nematode Phasmarhabditis hermaphrodita associates with complex and variable bacterial assemblages that do not affect its virulence. Journal of invertebrate pathology, 104(3), 222-226. When infected by P. hermaphrodita both morphological and behavioural characteristics of the slug change.
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There are over 40 antibiotic resistance genes identified on cassettes, as well as virulence genes. Transposons do not always excise their elements precisely, sometimes removing the adjacent base pairs; this phenomenon is called exon shuffling. Shuffling two unrelated exons can create a novel gene product or, more likely, an intron.
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In the case of chronically infected pigs, pleural adhesions and abscesses are normally found. Histological studies of infected lung tissue normally showcase lung necrosis, neutrophil infiltration, macrophage and platelet activation, and an exudate. Severe hemolysis or hemorrhaging is also present. Several virulence factors account for the remarkable pathogenicity of A. pleuropneumoniae.
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Each serotype expresses different amounts of the four Apx toxins. The most virulent combination known to exist, ApxI and ApxII, is expressed by serovars 1, 5, 9, and 11. The ApxII and ApxIII combination is of medium virulence and is expressed by serovars 2, 3, 4, 6, 8, and 15.
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Lipomannan is a mycobacterium immune agonist. In addition, it is a major constituent of the mycobacterium cell wall. This glycoconjugate is a virulence factor that plays a key role in the human immune system via interaction with various immune cells. It is also considered to be a precursor of lipoarabinomannans.
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Bacterial neuraminidase is type of neuraminidase and a virulence factor for many bacteria including Bacteroides fragilis and Pseudomonas aeruginosa. Its function is to cleave a sialic acid residue off ganglioside-GM1 (a modulator of cell surface and receptor activity) turning it into asialo-GM1 to which type 4 pili (attachment factors) bind preferentially.
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When only one bacterium could kill the other, the other strain was excluded by the competition. But when caterpillars were infected with bacteria both of which had toxins able to kill the other strain, neither strain was excluded, and their virulence was less than when the insect was infected by a single strain.
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A case of phaeophyphomycosis caused by a new species of Philaphora. Mycologia 66:490-498 Phaeohyphomycosis is an uncommon infection, however the number of case reported has been increasing in recent years. Fungal melanin is thought to be a virulence factor. The outcome of antifungal treatment is poor, and mortality is almost 80%.
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At this time, no studies demonstrate genome-wide rearrangement events directly giving rise to pathogenic behavior in a microbe. This does not mean it is not possible. Genome-wide rearrangements do, however, contribute to the plasticity of bacterial genome, which may prime the conditions for other factors to introduce, or lose, virulence factors.
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Nevertheless, he wondered whether the Penicillium might have weakened the bacteria before the mold perished.(Duchesne, 1897), p. 37: " … mais rien ne dit qu'avant de périr elles n'aient porté une atteinte quelconque à la virulence des microbes et peut-être à leurs propriétés pathogènes." ( … but nothing says that before perishing, they [i.e.
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A Polysaccharide Virulence Factor of a Human Fungal Pathogen Induces Neutrophil Apoptosis via NK Cells. Journal of Immunology. 192(11):5332-42 and reduce inflammation. Gresnigt, M.S., Bozza, S., Becker, K.L., Joosten, L.A., Abdollahi-Roodsaz, S., van der Berg, W.B., Dinarello, C.A., Netea, M.G., Fontaine, T., De Luca, A., et al. (2014).
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Originally identified as a regulator of genes involved in nitrogen metabolism and assimilation under nitrogen limiting conditions, E. coli σ54 has since been shown to play important regulatory roles in a variety of other cellular processes. Similarly, σ54 homologues in other species regulate a wide range of processes, including flagellar synthesis and virulence.
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The slug parasitic nematode Phasmarhabditis hermaphrodita associates with complex and variable bacterial assemblages that do not affect its virulence. Journal of invertebrate pathology, 104(3), 225-226. Reproduction occurs and the next generation continues to reproduce until food runs out and more third stage infective dauers are produced and the cycle is repeated.
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Protease effector AvrRpt2 is able to degrade RIN4, causing de-repression of RPS2. On the other hand, AvrB or AvrRPM1-mediated phosphorylation of RIN4 results in activation of RPM1. In short, this example elucidates how one NBS- LRR protein is able to recognize the effects of more than one virulence factor or effector.
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Numerous bacterial small noncoding RNAs have been identified to play regulatory functions. Some can regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the Y. pestis sRNA-ome. Among them was Yersinia-specific (also present in Y. pseudotuberculosis and Y. enterocolitica) Ysr141 (Yersinia small RNA 141).
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Another study uncovered that a temperature-induced global reprogramming of central metabolic functions are likely to support intestinal colonization of the pathogen. Environmentally controlled regulatory RNAs coordinate control of metabolism and virulence allowing rapid adaptation and high flexibility during life-style changes. High-throughput RNA structure probing identified many thermoresponsive RNA structures.
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Examples of viruses with similar amino acid identity include suipoxvirus, yatapoxvirus, and leporipoxvirus. In terminal regions, however, collinearity is interrupted. In these regions, poxvirus homologues are either absent or share a lower percentage of amino acid identity. Most of these differences involve genes that are likely associated with viral virulence and host range.
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The active site of Cif is shown with a Cα trace in gray, and side chains of select residues playing a role in catalysis are displayed as sticks. From . Cif is an epoxide hydrolase (EH) with unique substrate selectivity. Cif is the first example of an EH serving as a virulence factor.
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VrrA (Vibrio regulatory RNA of OmpA) is a non-coding RNA that is conserved across all Vibrio species of bacteria and acts as a repressor for the synthesis of the outer membrane protein OmpA. This non-coding RNA was initially identified from Tn5 transposon mutant libraries of Vibrio cholerae and its location within the bacterial genome was mapped to the intergenic region between genes VC1741 and VC1743 by RACE analysis. Outer membrane vesicles are secreted from the surface of gram-negative bacteria, where they are thought to aid in virulence. Little is known about how these vesicles aid virulence but it has been speculated that they may contribute by secreting toxins and help in the evasion of the immune system.
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In cultured cells, InlA is necessary to facilitate Listeria entry into human epithelial cells, while InlB is necessary for Listeria internalisation in several other cell types, including hepatocytes, fibroblasts, and epithelioid cells. Internalins are mainly surface-exposed virulence factors present in a number of Gram-positive bacteria whose role ranges from recognition of cellular receptors to aid in pathogen entry to escape from autophagy.Structure of Internalin InlK from the Human Pathogen Listeria monocytogenes Listeria poses a particular threat to pregnant women because of its ability to cross the placental blood barrier through the combined binding of both InIA and InIB to host cells. Research has shown that only the combined binding of these two virulence factors allows the bacteria to cross that barrier.
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By inserting separate, successive sections of V. cholerae DNA into the DNA of other bacteria, such as E. coli that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which V. cholerae responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered a complex cascade of regulatory proteins controls expression of V. cholerae virulence determinants. In responding to the chemical environment at the intestinal wall, the V. cholerae bacteria produce the TcpP/TcpH proteins, which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of virulence genes that produce the toxins, causing diarrhea in the infected person and allowing the bacteria to colonize the intestine.
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Hogenhout's research looks at the interactions between insects and plants and how microorganisms can manipulate this. Her group discovered the key virulence protein SAP54 which phytoplasma bacteria use to manipulate the flowering of plants, the bacteria is carried between plants by plant feeding insects such as leafhoppers. Her work looks at other insects that transmit plant diseases such as the peach potato aphid Myzus persicae, this aphid can carry many different plant viruses and feeds on a wide range of plants and can manipulate plants to benefit the aphids by producing virulence proteins. Her group have sequenced the genome of the peach potato aphid and were surprised to find that it was smaller than the pea aphid Acyrthosiphon pisum, a species with many fewer host plants.
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Among chromosomal protein-coding genes, their nucleotide genomic identity rates 97%. They are different in terms of their virulence potential and transmission mechanisms. Y. pestis is not a human- adapted bacteria. Its main reservoirs are rodents (like marmots, mice, great gerbils, voles and prairie dogs) and it is transmitted to humans by the flea.
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A homologous domain is found in YscM (Yop secretion protein M), which acts as a Yop protein translocation protein. Several Yop proteins are involved in pathogenesis. YscM is produced by the virulence operon virC, which encodes thirteen genes, yscA-M. Transcription of the virC operon was subjected to the same regulation as the yop genes.
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NDV strains can be categorised as velogenic (highly virulent), mesogenic (intermediate virulence), or lentogenic (nonvirulent). Velogenic strains produce severe nervous and respiratory signs, spread rapidly, and cause up to 90% mortality. Mesogenic strains cause coughing, affect egg quality and production, and result in up to 10% mortality. Lentogenic strains produce mild signs with negligible mortality.
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In 1882, Pasteur sent his assistant Louis Thuillier to southern France because of an epizootic of swine erysipelas. Thuillier identified the bacillus that caused the disease in March 1883. Pasteur and Thuillier increased the bacillus's virulence after passing it through pigeons. Then they passed the bacillus through rabbits, weakening it and obtaining a vaccine.
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Notions would first collect "matter" – i.e., smallpox pus. He would then dry it using peat smoke (which was believed to lessen the virus's virulence), and bury it in the ground with camphor (which has anti-bacterial properties, preventing the matter from decomposing). Oral history indicates the matter was spread between glass sheets before burial.
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In molecular biology, Vibrio cholerae ToxT activated RNAs are small RNAs which are produced by the bacterium Vibrio cholerae. They are regulated by the transcriptional activator ToxT and may play a role in V. cholerae virulence. Two ToxT activated RNAs have been described: TarA (ToxT activated RNA A) and TarB (ToxT activated RNA B).
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These proteins are coded for by genes in chromosomal DNA, bacteriophage DNA or plasmids. Certain bacteria employ mobile genetic elements and horizontal gene transfer. Therefore, strategies to combat certain bacterial infections by targeting these specific virulence factors and mobile genetic elements have been proposed. Bacteria use quorum sensing to synchronise release of the molecules.
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A characteristic central feature of meiosis is recombination between homologous chromosomes. This process is associated with repair of DNA damage, particularly double-strand breaks. The ability of C. neoformans and U. maydis to undergo meiosis may contribute to their virulence by repairing the oxidative DNA damage caused by their host's release of reactive oxygen species.
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Bacterial pili are hair-like surface-exposed organelles. They are responsible for recognition of and attachment to the host and thus, are also crucial virulence factors. Pili are polymer of protein subunits, the assembly of which requires accessory proteins. The Waksman lab engages in research on pili assembled by the Chaperone-Usher (CU) pathway.
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Jurkat J6 cells have been found to produce a xenotropic murine leukemia virus (X-MLV) (referred to as XMRV) that could potentially affect experimental outcomes. There is no evidence that this virus can infect humans. This infection may also change the virulence and tropism of the virus by way of phenotypic mixing and/or recombination.
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It is then directed into the nucleus via interactions with the host cell proteins such as importin a, bacterial VirE3, and dynein-like proteins. Several other bacterial virulence effectors like VirB5, VirB7 (the minor components of the T-complex), VirD5, VirE2, VirE3, and VirF that may also interact with proteins of host plant cells.
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This sample is marked "RISE505". This strain's genes express flagellin, which triggers the human immune response. However, by contrast with other prehistoric Yersinia pestis bacteria, the strain does so weakly; later, historic plague does not express flagellin at all, accounting for its virulence. The Kytmanovo strain was therefore under selection toward becoming a plagueRasmussen, 575.
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She discovered that, instead, surface polysaccharides were responsible for their virulence factor. During World War II, Lancefield served on the Commission on Streptococcal and Staphylococcal Diseases of the Armed Forces Epidemiological Board. In 1946, Lancefield was promoted to associate member at Rockefeller University. She was promoted to full member and professor at Rockefeller in 1958.
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Some of the best-known examples of quorum sensing come from studies of bacteria. Bacteria use quorum sensing to regulate certain phenotype expressions, which in turn, coordinate their behaviours. Some common phenotypes include biofilm formation, virulence factor expression, and motility. Certain bacteria are able to use quorum sensing to regulate bioluminescence, nitrogen fixation and sporulation.
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The fim switch in Escherichia coli is the mechanism by which the fim gene cluster, encoding Type I Pili, is transcriptionally controlled. These pili are virulence factors involved in adhesion, especially important in uropathogenic Escherichia coli. The gene undergoes phase variation mediated via two recombinases and is a model example of site specific inversion.
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Oxygen radicals react with plant cell lipids, proteins, and nucleic acids, damaging and killing affected cells, and nutrients released during the cell rupture and death feed the Cercospora fungus. A study of mutant Cercospora lacking the gene responsible for cercosporin production demonstrates that, though unnecessary for infection, cercosporin increases the virulence of Cercospora fungi.
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Peng, D., Chai, L., Wang, F., Zhang, F., Ruan, L., and Sun, M. (2011) "Synergistic activity between Bacillus thuringiensis Cry6Aa and Cry55Aa toxins against Meloidogyne incognita". Microbial biotechnology. 4, 794-798Luo, X., Chen, L., Huang, Q., Zheng, J., Zhou, W., Peng, D., Ruan, L. and Sun, M., 2013. "Bacillus thuringiensis metalloproteinase Bmp1 functions as a nematicidal virulence factor".
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This toxin has been shown to be the key virulence factor in infection with C. perfringens; the bacterium is unable to cause disease without this toxin. Further, vaccination against the alpha toxin toxoid protects mice against C. perfringens gas gangrene. As a result, knowledge about the function of this particular protein greatly aids understanding of myonecrosis.
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Kumamoto has also studied candida auris a fungus that was identified in 2009 that appears to withstand anti-fungal drugs. She is interested in the mechanism by which C. albicans interacts with its host during colonisation and invasive degrees. For example, Kumamoto has demonstrated that the interaction of C. albicans with other pathogens can influence its virulence.
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The first case is that of the sortases, an enzyme family that is spread throughout numerous gram positive bacteria. It has been shown to be an important pathogenicity and virulence factor. The general reaction performed by sortases involves using its own brand of the ‘catalytic triad’: i.e. using histidine, arginine, and cysteine for the reactive mechanism.
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In addition to the ampliPHOX Colorimetric Detection Technology, InDevR also supplies Custom Low Density Microarrays specifically designed to work with the ampliPHOX platform. The Custom Microarrays can include up to 850 unique probes per array. Research at the USDA has utilized ampliPHOX to profile Shiga toxin- producing Escherichia coli by identifying the O-antigen gene clusters and virulence genes.
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One of these tests involved growth on cysteine-glucose-blood agar (CGBA). F. tularensis took 2 to 7 days to appear on the CGBA, while F. novicida took only 24 hours to appear. F. novicida grows much more rapidly on CGBA than F. tularensis. Another difference between the two is the virulence of F. novicida was lower.
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Virulence is the second full-length studio album from melodic hardcore band, Only Crime. It was released on January 23, 2007 and features the same line-up as the previous album, To the Nines, including Russ Rankin from Good Riddance, Bill Stevenson from Black Flag, Descendents and ALL, Aaron Dalbec from Bane, and the Blair Brothers from Hagfish.
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The 1892 outbreak in Hamburg, Germany was the only major European outbreak; about 8,600 people died in that city. Although many residents held the city government responsible for the virulence of the epidemic (leading to cholera riots in 1893), it continued with practices largely unchanged. This was the last serious European cholera outbreak of the century.
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SAP11 effectors are identified in a number of divergent phytoplasmas and these effectors also interact with TCPs and modulate plant defenses. SAP11 is the first phytoplasma virulence protein for which plant targets and effector functions (i.e. evidence of benefit for the pathogen) were identified. TCPs were found to be targeted by a number of other pathogen effectors.
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These "toxins" allow the further spread of bacteria and, as a consequence, deeper tissue infections. Examples are hyaluronidase and collagenase. These molecules, however, are enzymes that are secreted by a variety of organisms and are not usually considered toxins. They are often referred to as virulence factors, since they allow the organisms to move deeper into the hosts tissues.
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Wallace, D. E. E., J. G. V. Asensio, and A. A. P. Tomas. "Correlation between Virulence and Genetic Structure of Escovopsis Strains from Leaf-Cutting Ant Colonies in Costa Rica." Microbiology-Sgm 160 (2014): 1727–36. Leafcutter ants communicate through exchanges of chemicals and secrete chemicals made from actinomycete bacteria in order to protect their colonies.
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A study published in the American Journal of Gastroenterology found that to control the spread of CDIs glove use, hand hygiene, disposable thermometers and disinfection of the environment are necessary practices in health facilities. The virulence of this pathogen is remarkable and may take a radical change at sanitation approaches used in hospitals to control CDI outbreaks.
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To effectively achieve adherence to host surfaces, many bacteria produce multiple adherence factors called adhesins. Bacterial adhesins provide species and tissue tropism. Adhesins are expressed by both pathogenic bacteria and saprophytic bacteria. This prevalence marks them as key microbial virulence factors in addition to a bacterium's ability to produce toxins and resist the immune defenses of the host.
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Cultures of human lung epithelial cells incubated with anti-alpha-toxin and infected with S. aureus showed marked reductions in cellular damage when compared to control cells. As many strains of S. aureus are proving to be resistant to most available antibiotics, specific targeting of virulence factors with antibodies may be the next step to treating this pathogen.
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These attempts increased the virulence of the virus. Then, he realized that he could put dog tissue into a monkey to infect it and then perform serial passage in monkeys. After completing this process and infecting a dog with the resulting virus, Pasteur realized that the virus was less virulent. Mostly, Pasteur worked with the rabies virus in rabbits.
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In bacteria and fungi, exoenzymes play an integral role in allowing the organisms to effectively interact with their environment. Many bacteria use digestive enzymes to break down nutrients in their surroundings. Once digested, these nutrients enter the bacterium, where they are used to power cellular pathways with help from endoenzymes. Many exoenzymes are also used as virulence factors.
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Parkhill uses high throughput sequencing and phenotyping to study pathogen diversity and variation, how they affect virulence and transmission, and what they tell us about the evolution of pathogenicity and host–pathogen interaction. Research in the Parkill Laboratory has been funded the Wellcome Trust, the Biotechnology and Biological Sciences Research Council (BBSRC) and the Medical Research Council (MRC).
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Fungal-farming in a snail. Proc. Natl. Acad. Sci. 100:15643–48. In coastal New England, this evidence is weaker. Certain fungal pathogens of S. alterniflora were found more frequently in sites of die-off. These pathogens have varying degrees of virulence, and there is some evidence of association with species of Fusarium and areas of die-off.
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This mechanism is a common source of new genes in prokaryotes, sometimes thought to contribute more to genetic variation than gene duplication. It is a common means of spreading antibiotic resistance, virulence, and adaptive metabolic functions. Although horizontal gene transfer is rare in eukaryotes, likely examples have been identified of protist and alga genomes containing genes of bacterial origin.
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Ayres, B. Drummond, "Miami Votes 2 to 1 to Repeal Law Barring Bias Against Homosexuals", The New York Times, p. 23. National Gay Task Force (NGTF) co-director Jean O'Leary said that the result was "all the evidence anyone could need of the extent and virulence of prejudice against lesbians and gay men in our society".
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RNA-TGB is a gene with 4 open reading frames (ORFs); the first three overlapping ORFs form an area called the triple gene block. This 3 frame block codes for essential movement factor proteins that facilitate cell-to-cell movement. The fourth ORF codes for another cysteine- rich protein that increases virulence and has some RNA silencing suppressive activity.
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Of these MSPs, MSP1 and MSP2 are primarily responsible for avoiding immune cells. The virulence of P. falciparum is mediated by erythrocyte membrane proteins, which are produced by the schizonts and trophozoites inside the erythrocytes and are displayed on the erythrocyte membrane. PfEMP1 is the most important, capable of acting as both an antigen and an adhesion molecule.
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Zuckerberg has spoken out against social media, arguing that it has created a toxic culture and given men 'with anti-feminist ideas to broadcast their views to more people than ever before – and to spread conspiracy theories, lies and misinformation'. Zuckerberg understands that social media has elevated misogyny to 'entirely new levels of violence and virulence'.
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The cagA gene codes for one of the major H. pylori virulence proteins. Bacterial strains with the cagA gene are associated with an ability to cause ulcers. The cagA gene codes for a relatively long (1186-amino acid) protein. The cag pathogenicity island (PAI) has about 30 genes, part of which code for a complex type IV secretion system.
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Microbialized coral reefs have relatively high bacteria abundances and reduced bacteriophage abundances. To explain this observation, Rohwer and colleagues (Knowles et al. 2016) proposed that the temperate life cycle was the predominant bacteriophage life cycle at high host abundances. The resulting bacterial lysogens would be protected from other bacteriophage via superinfection exclusion and protists via expression of virulence factors.
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Virulence is a peer-reviewed medical journal that covers microbiology and immunology specifically, microorganism pathogenicity, the infection process and host–pathogen interactions. It is a fully Open Access journal published by Taylor & Francis. It was previously published 8 times per year by Landes Bioscience. The journal was established in 2010 by Eva M. Riedmann, and Eleftherios Mylonakis.
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Heme is an abundant source of iron in the human host, and P. aeruginosa is the only Pseudomonas species capable of causing infection in humans. Therefore, it is hypothesized that the PrrH RNA plays a role in P. aeruginosa's adaptability as a human pathogen. Both homologues inhibit translation of antR mRNA, which affects quorum sensing and virulence factor production.
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The PhoPQ two-component system is repressed by MicA. The RNA presumably pairs with the ribosomal binding site of phoP mRNA, thereby inhibiting translation. This links micA to cellular processes such as Mg(2+) transport, virulence, LPS modifications and resistance to antimicrobial peptides. In S. typhimurium MicA has been shown to be involved in biofilm formation.
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HRG has also been shown to inhibit the M2-like phenotype of tumor-associated macrophages. In addition, HRG has been discovered to play a role in infection. Some studies have found HRG has the antibacterial activity against Streptococcus pyogenes and a direct interaction between a S. pyogenes virulence factor (sHIP) and the human HRG has been identified.
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The genome for B. mallei is made up of two circular chromosomes. Chromosome 1 is where genes relating to metabolism, capsule formation, and lipopolysaccharide biosynthesis are located. B. mallei has a polysaccharide capsule which indicates its potential as a pathogen. Chromosome 2 is where most of the information regarding secretion systems and virulence-associated genes are located.
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There has long been uncertainty over how viroids induce symptoms in plants without encoding any protein products within their sequences. Evidence suggests that RNA silencing is involved in the process. First, changes to the viroid genome can dramatically alter its virulence. This reflects the fact that any siRNAs produced would have less complementary base pairing with target messenger RNA.
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Some of the inhibitory effects include distance, physical barriers and host defenses. These inhibitory effects may differ among individuals due to the inhibitory effects being genetically controlled. Viral pathogenesis is affected by various factors: (1) transmission, entry and spread within the host, (2) tropism, (3) virus virulence and disease mechanisms, (4) host factors and host defense.
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Sclerotinia gemycircularvirus 1 is a single stranded DNA virus with a circular genome that infects the fungus Sclerotinia sclerotiorum. Infection with this virus decreases the virulence of this fungus. The mechanism of this effect is not known. Although a number of viruses infect fungi, this virus is the only known example of a DNA virus infecting a fungus.
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In epidemiology, infectivity is the ability of a pathogen to establish an infection. More specifically, infectivity is a pathogen's capacity for horizontal transmission that is, how frequently it spreads among hosts that are not in a parent-child relationship. The measure of infectivity in a population is called incidence. Infectivity has been shown to positively correlate with virulence.
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Avian trichomoniasis is principally a disease of young birds. T. gallinae varies greatly in its virulence. The severity of the disease depends on the susceptibility of the bird and on the pathogenic potential of the strain of the parasite. Adult birds that recover from the infection may still carry the parasite, but are resistant to reinfection.
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When the disease is transferred to a new host, there is a delay in virulence, known as parasitic fitness. In maize, the reproductive tassels are malformed. The disease seems to stimulate growth while suppressing it in other areas of development: the anthers are atrophied while the female structure development is blocked. The resulting pollen is hollow and wrinkled.
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Teg49 is a non-coding RNA present in the extended promoter region of the staphylococcal accessory regulator sarA. It was identified by RNA-seq and confirmed by Northern blot. It is modulated by sigB (sarA regulator) and cshA (an ATP-dependant DEAD box RNA helicase) and it most likely contributes to virulence of S. aureus by modulating SarA expression.
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B. cereus bacteria are facultative anaerobes, and like other members of the genus Bacillus, can produce protective endospores. Its virulence factors include cereolysin and phospholipase C. The Bacillus cereus group comprises seven closely related species: B. cereus sensu stricto (referred to herein as B. cereus), B. anthracis, B. thuringiensis, B. mycoides, B. pseudomycoides, and B. cytotoxicus.
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Although poorly understood, it is believed that Nef is a primary cause for the destruction of SERINC5 and other restriction factors. When in the presence of virulence factors, specifically Nef, both SERINC5 and CD4 cells are downregulated through lysosomal degradation via the AP-2 endocytic pathway. This causes rapid infectivity, and an increase in viral load.
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Due to the significant correlations identified between hypoxia, fungal infections, and negative clinical outcomes, the mechanisms by which A. fumigatus adapts in hypoxia is a growing area of focus for novel drug targets. Two highly characterized sterol- regulatory element binding proteins, SrbA and SrbB, along with their processing pathways, have been shown to impact the fitness of A. fumigatus in hypoxic conditions. The transcription factor SrbA is the master regulator in the fungal response to hypoxia in vivo and is essential in many biological processes including iron homeostasis, antifungal azole drug resistance, and virulence. Consequently, the loss of SrbA results in an inability for A. fumigatus to grow in low iron conditions, a higher sensitivity to anti-fungal azole drugs, and a complete loss of virulence in IPA (invasive pulmonary aspergillosis) mouse models.
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The T-DNA fragment is flanked by 25-bp direct repeats, which act as a cis element signal for the transfer apparatus. The process of T-DNA transfer is mediated by the cooperative action of proteins encoded by genes determined in the Ti plasmid virulence region (vir genes) and in the bacterial chromosome. The Ti plasmid also contains the genes for opine catabolism produced by the crown gall cells, and regions for conjugative transfer and for its own integrity and stability. The 30 kb virulence (vir) region is a regulon organized in six operons that are essential for the T-DNA transfer (virA, virB, virD, and virG) or for the increasing of transfer efficiency (virC and virE) (Hooykaas and Schilperoort, 1992; Zupan and Zambryski, 1995, Jeon et al.
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The virulence of the pathogen implies the production of polysaccharide capsular layer, and extracellular products, and is also depending on iron availability (Lopez- Doriga et al., 2000). The bacteria spreads via infected phagocytes, mainly macrophages. This spread can be rapid, and lethal effects may occur within a few days of challenge, affecting tissues containing large numbers of the pathogens (Evelyn, 1996).
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In biology, phase variation is a method for dealing with rapidly varying environments without requiring random mutation. It involves the variation of protein expression, frequently in an on-off fashion, within different parts of a bacterial population. As such the phenotype can switch at frequencies that are much higher (sometimes >1%) than classical mutation rates. Phase variation contributes to virulence by generating heterogeneity.
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The ability to form biofilms on plastic devices is a major virulence factor for S. epidermidis. One probable cause is surface proteins that bind blood and extracellular matrix proteins. It produces an extracellular material known as polysaccharide intercellular adhesin (PIA), which is made up of sulfated polysaccharides. It allows other bacteria to bind to the already existing biofilm, creating a multilayer biofilm.
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Viroporins can also be considered virulence factors; in viruses in which viroporins are not essential, their pathogenicity is attenuated in the absence of viroporin beyond the level expected by the effects on viral propagation. In some cases the membrane permeabilization effects of viroporins activate the inflammasome, a protein complex associated with activation of innate immunity which, when overactive, can cause disease symptoms.
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Secretion of the effectors is coordinated with expression of other virulence factors via shared regulatory networks. The effector repertoire has been proposed to be a determinant of host specificity. Xanthomonas actively kill other bacterial using type IV secretion system and defend itself from amoeba using type VI secretion system. To prevent infections, limiting the introduction of the bacteria is key.
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The results demonstrate that the virulence of infective endocarditis caused by S. mutans is linked to the specific cell surface components present. In addition, S. mutans DNA has been found in cardiovascular specimens at a higher ratio than other periodontal bacteria. This highlights its possible involvement in a variety of types of cardiovascular diseases, not just confined to bacteraemia and infective endocarditis.
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It has been demonstrated that aureolysin has impact for bacterial survival in human whole blood. Aureolysin is also up-regulated upon phagocytosis and promotes intracellular survival. S. aureus prefers to establish a chronic, or long lasting infection within a host. While promoting dissemination and counteracting immune mechanisms, aureolysin also regulates secreted virulence factors to control the pathogenicity of the bacterium.
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The higher incidence of mortality among males compared to females is not well understood, but is thought to be related to immunological differences across gender. The symptoms of syphilis have become less severe over the 19th and 20th century in part due to widespread availability of effective treatment and partly due to decreasing virulence of the spirochete. With early treatment few complications result.
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Gliotoxin is suspected to be an important virulence factor in Aspergillus fungus. Gliotoxin possesses immunosuppressive properties that may suppress and cause apoptosis in certain cells of the immune system, including neutrophils, eosinophils, granulocytes, macrophages, and thymocytes. Specifically, neutrophils exposed to gliotoxin release less reactive oxygen species (ROS) and complete fewer phagocytic activities. Gliotoxin is also believed to interfere with T-cell activation.
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Neoh is a microbiologist and a researcher. Neoh is interested in antimicrobial resistance and virulence of nosocomial pathogens, especially Staphylococcus aureus; diagnosis and pathogenesis of sepsis, gut microbiota in colorectal cancer, seroepidemiology of dengue and chikungunya generally in the Malaysian population. On 15 February 2017, Neoh was appointed as Deputy Director (Research, Innovation and Networking), Universiti Kebangsaan Malaysia until 14th February 2020.
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Several other types of lipase activities exist in nature, such as phospholipases and sphingomyelinases; however, these are usually treated separately from "conventional" lipases. Some lipases are expressed and secreted by pathogenic organisms during an infection. In particular, Candida albicans has many different lipases, possibly reflecting broad-lipolytic activity, which may contribute to the persistence and virulence of C. albicans in human tissue.
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The pathogenicity of Aeromonas species was believed to be mediated by a number of extracellular proteins such as aerolysin, lipase, chitinase, amylase, gelatinase, hemolysins, and enterotoxins. However, the pathogenic mechanisms are unknown. The recently proposed type-III secretion system (T3SS) has been linked to Aeromonas pathogenesis. T3SS is a specialized protein secretion machinery that exports virulence factors directly to host cells.
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Recently, Streptococcus dysgalactiae subspecies dysgalactiae has been described as an emerging pathogen in fish, causing fulminant necrotic ulcers of the caudal peduncle, with ensuing high mortality rates. The clinical presentation is dominated by severe sepsis and the formation of microabscesses, and a relationship between disease severity and the expression of the virulence factors Streptolysin S and SPEGdys has been inferred.
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Moreover, it has been suggested that GBS pigment and hemolysin are identical or closely related molecules and it has also been reported that they are important factors contributing to GBS virulence. Nevertheless, 1-5% of GBS strains are non-hemolytic and do not produce pigment., however these non-hemolytic and non-pigmented GBS strains (lacking pigment and hemolysin) are considered less virulent.
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Elastase breaks down elastin, an elastic fibre that, together with collagen, determines the mechanical properties of connective tissue. The neutrophil form breaks down the Outer membrane protein A (OmpA) of E. coli and other Gram-negative bacteria. Elastase also has the important immunological role of breaking down Shigella virulence factors. This is accomplished through the cleavage of peptide bonds in the target proteins.
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Lpp, along with another OmpA-like lipoprotein called Pal/OprL (), maintains the stability of the cell envelope by attaching the outer membrane to the cell wall. Lpp has been proposed as a virulence factor of Yersinia pestis, the cause of plague. Y. pestis needs lpp for maximum survival in macrophages and to efficiently kill mouse models of bubonic and pneumonic plague.
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One benefit of meiosis in C. neoformans could be to promote DNA repair in the DNA-damaging environment caused by the oxidative and nitrosative agents produced in macrophages. Thus, C. neoformans can undergo a meiotic process, monokaryotic fruiting, that may promote recombinational repair in the oxidative, DNA-damaging environment of the host macrophage, and this may contribute to its virulence.
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The N-terminal portion of the mature protein is thought to be responsible for chloramphenicol sensitivity. Also, they induce activation of several signal transduction cascades, including activation of PI-3 kinase. The Dr family of adhesins are particularly associated with cystitis and pregnancy-associated pyelonephritis.Identified Virulence Factors of UPEC : Adherence, State Key Laboratory for Moleclular Virology and Genetic Engineering, Beijing.
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Among other virulence-related enzymes, T. tonsurans also produces urease. This fungus has also been found to produce melanin, which may be phenotypically demonstrated through in vitro induction in caffeic acid media. Melanin acts as an antioxidant molecule, providing protective properties to the fungus from damaging UV rays. Since it is endemic in sunny regions, the melanin production is perhaps crucial for survival.
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These virulence phenotypes range from thicker biofilms to allowing them to grow in a variety of environments including medical devices such as urinary catheters and prosthetic heart valves within the body. The thicker biofilms act as a “mechanical and biochemical shield” that protects the bacteria from the antibiotics and are the most effective protective mechanism that bacteria have against treatment.
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Some of these X. campestris sRNAs are only found in Xanthomonas, some are also expressed in other bacteria. Several of these sRNAs appear to contribute to virulence, including sX12, sX13 and sRNA-Xcc1. Computational analysis predicts 63 sRNAs in Xanthomonas oryzae pathovar oryzae, expression of 8 of these has been experimentally confirmed. Expression of three of these is Hfq-dependent.
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Granulotomatous lesions are important in both regulating the immune response and minimizing tissue damage. Moreover, T cells help maintain Mycobacterium within the granulomas. The ability to construct M. tuberculosis mutants and test individual gene products for specific functions has significantly advanced the understanding of its pathogenesis and virulence factors. Many secreted and exported proteins are known to be important in pathogenesis.
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L. monocytogenes also senses the entry to host by examining available nutrient sources. For example L-glutamine, an abundant nitrogen source in the host, induces the expression of virulence genes in L. monocytogenes. Little is known about how this bacterium switches between acting as a saprophyte and a pathogen; however, several noncoding RNAs are thought to be required to induce this change.
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An alien also escapes and at the same time an airborne virus sealed in the shell kills four members of the scientific team by melting them from within. The virus also kills all the plants, making them wilt and turn brown. The virus has an unusually high speed of transmission and extreme virulence. It kills anyone within a few minutes of exposure.
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Threats include habitat loss, competition with colonial honeyeaters, especially the Noisy Miner, and parasitism. The Tasmanian ectoparasite, Passeromyia longicornis demonstrates a higher parasite load and virulence with high nestling mortality in Forty-spotted Pardalote nests compared to Striated Pardalotes. Over the 2-year study by Edworthy et al., Forty-spotted Pardalotes fledged fewer nestlings (18%) than sympatric Striated Pardalotes (26%).
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It also counteracts the host cell antiviral response and seems to be the main virulence factor,Kohl A, Clayton RF, Weber F, Bridgen A, Randall RE, et al. (2003) Bunyamwera virus nonstructural protein NSs counteracts interferon regulatory factor 3-mediated induction of early cell death. J Virol 77: 7999–8008. acting at the level of transcription by inhibiting RNA polymerase II–mediated transcription.
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Providencia rettgeri is a natural pathogen of Drosophila fruit flies. Susceptibility to P. rettgeri is strongly tied to an allele of the antimicrobial peptide gene Diptericin. The fly's defence against P. rettgeri seems to rely almost exclusively on Diptericin, as deletion of Diptericin leads to complete mortality. Meanwhile deletion of multiple other antimicrobial peptides has no effect on P. rettgeri virulence.
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He subsequently served at Ratnagiri, and Mumbai, and was appointed Vice-Principal of the Training College at Poona. From Poona he was posted to Solapur as headmaster of the high school in 1890. He worked at Solapur for eight years. In 1897, the plague broke out at Solapur in all its virulence and Government opened out its operation in vigour.
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Pathogenic Leptospira spp. has features of both a gram-positive and gram-negative pathogen. Features of the gram-negative pathogen is the presences of lipopolysaccharides (LPS), but the closeness of the cytoplasmic membrane to the cell wall shows more of a gram-positive feature. Also, the virulence factors on the flagella of pathogenic leptospires have thought to be involved in the overall infection.
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The clinical signs displayed are dependent on the virulence of the strain. There is a vaccine available which reduces the severity and incidence of disease. Some countries in Europe have successfully eradicated the disease by applying a strict culling policy. Infection can occur in cattle of any age, but it is most commonly seen between the ages of 6 and 18 months.
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The production of SHP's increases biofilm biogenesis. It has been suggested that GAS switches between biofilm formation and degradation by utilizing pathways with opposing effects. Whilst Rgg2/3 pathway increases biofilm, the RopB pathway disrupts it. RopB is another Rgg-like protein (Rgg1) that directly activates SpeB (Streptococcal pyrogenic exotoxin B), a cysteine protease that acts as a virulence factor.
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Diphtheria toxin is an exotoxin secreted by Corynebacterium, the pathogenic bacterium that causes diphtheria. The toxin gene is encoded by a prophage (a virus that has inserted itself into the genome of the host bacterium).TABLE 1. Bacterial virulence properties altered by bacteriophages from The toxin causes the disease in humans by gaining entry into the cell cytoplasm and inhibiting protein synthesis.
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Nelfinavir and simple derivatives have been found to inhibit the production of the virulence factor streptolysin S, a cytolysin produced by the human pathogen Streptococcus pyogenes. Nelfinavir and these related molecules did not exhibit detectable antibiotic activity, but did also inhibit the production of other biologically active molecules, including plantazolicin (antibiotic), listeriolysin S (cytolysin), and clostridiolysin S (cytolysin), by other bacteria.
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Some in the late stage also showed increased antithrombin. This form of smallpox occurred in anywhere from 3 to 25 percent of fatal cases, depending on the virulence of the smallpox strain. Cases with flat lesions had a higher fatality rate than those with raised pustular lesions. Most people with the late stage form died within 8 to 12 days of illness.
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Much is unknown about the pathogenecity and virulence of Yokose virus including in bats. The strain XYBX1332 isolated in China was found to cause cytopathic effects in mammalian cells. In the study of fruit bats infected with Yokose virus, they did not observe any clinical signs of disease. Currently only species of bats have been identified of carrying Yokose viral strains.
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Clostridium species produce more toxins and exhibit higher degrees of virulence than any other bacterial taxon. Clostridium infections are usually opportunistic, and occur in individuals with serious preexisting medical conditions. However, Clostridium infections are also known to occur in healthy individuals. Four species of Clostridium (Clostridium botulinum, Clostridium perfringens, Clostridium tetani, and Clostridium sordelli) are responsible for most human infections.
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In 1999, the virulence genes associated with Mycobacterium tuberculosis were identified through transposon mutagenesis-mediated gene knockout. A plasmid named pCG113 containing kanamycin resistance genes and the IS1096 insertion sequence was engineered to contain variable 80-base pair tags. The plasmids were then transformed into M. tuberculosis cells by electroporation. Colonies were plated on kanamycin to select for resistant cells.
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SaPIs were found to carry the gene encoding toxic shock syndrome toxin. Other SaPI subtypes have been found to provide host Staphylococcus strains with the ability to coagulate animal host blood plasma by coding for different alleles of a von Willebrand factor- binding protein. This virulence factor may help S. aureus adapt to distinct animal hosts such as horses or ruminants.
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TB has a very high level of virulence which is mainly due in part to the fact it is extremely transmissible. TB was considered one of the most prevalent diseases, and did not have a cure until the discovery of streptomycin by Selman Waksman in 1943. However, the bacteria soon developed resistance. Since then, drugs such as isoniazid and rifampin have been used.
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A sharp rise in mortality is often seen (depending on the virulence of the disease). Other clinical signs include abdominal swelling, anorexia, abnormal swimming, darkening of the skin, and trailing of the feces from the vent. On necropsy, internal damage (viral necrosis) to the pancreas and thick mucus in the intestines often is present. Surviving fish should recover within one to two weeks.
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This shows true virulence genes may only be expressed during the early stages of infection.Boyce, JD. How does P. multocida respond to the host environment? “Current Opinion in Microbiology” vol.9 no.1 (117-122) Genetic transformation is the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipient’s genome.
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A Bacillus cereus cell that has undergone filamentation following antibacterial treatment (upper electron micrograph; top right) and regularly sized cells of untreated B. cereus (lower electron micrograph) Filamentation is the anomalous growth of certain bacteria, such as Escherichia coli, in which cells continue to elongate but do not divide (no septa formation). The cells that result from elongation without division have multiple chromosomal copies. In the absence of antibiotics or other stressors, filamentation occurs at a low frequency in bacterial populations (4-8% short filaments and 0-5% long filaments in 1- to 8-hour cultures), the increased cell length protecting bacteria from protozoan predation and neutrophil phagocytosis by making ingestion of the cells more difficult. Filamentation is also a virulence factor thought to protect bacteria from antibiotics, and is associated with other aspects of bacterial virulence such as biofilm formation.
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His lab established that humoral immunity could protect against intracellular pathogens, demonstrated that Cryptococcus neoformans was a facultative intracellular pathogen, and suggested that virulence in environmental fungi was selected by amoeba predators, a hypothesis dubbed "accidental virulence". Jointly with British biologist Robin May, his group were the first to observe non-lytic expulsion, or vomocytosis, of intracellular fungi. Subsequently, with Kirsten Nielsen at the University of Minnesota, he characterized the ability of cryptococci to form "giant" or "titan" cells in vivo, unusually large cells that help drive persistent infections. His lab continues to work on fungal and bacterial pathogenesis. Together with Liise-anne Pirofski, he proposed the ‘Damage- Response Framework’ of microbial pathogenesis, a new synthesis that shifted the emphasis away from focusing on microbes as pathogens, commensals, opportunists to the outcome of host-pathogen interactions.
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Campylobacteriosis seems to be dependent on several virulence factors involving adhesion, invasion and bacterial motility adherence. Campylobacter secrete a cytolethal distending toxin (CDT), which is an AB toxin composed of three subunits encoded by cdtA, cdtB and cdtC. This toxin has DNase activity, which causes DNA double-strand breaks during the cell cycle G2 phase, leading eventually to cell apoptosis in HeLa and Caco-2 cells.
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They are typically 20–30 μm long and 0.2–0.3 μm wide. Spirochetes move using axial filaments called endoflagella in their periplasmic space. The filaments rotate in this space, between the outer membrane and the peptidoglycan layer, propelling the bacterium forward in a corkscrew-like motion. The outer membrane of Borrelia species contains outer surface proteins (Osp) that play a role in their virulence.
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Nucleotide sugar metabolism is particularly well-studied in yeast, fungal pathogens, and bacterial pathogens, such as E. coli and Mycobacterium tuberculosis, since these molecules are required for the synthesis of glycoconjugates on the surfaces of these organisms. These glycoconjugates are virulence factors and components of the fungal and bacterial cell wall. These pathways are also studied in plants, but here the enzymes involved are less well understood.
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Bacterial small RNAs play important roles in many cellular processes; 11 small RNAs have been experimentally characterised in E. faecalis V583 and detected in various growth phases. Five of them have been shown to be involved in stress response and virulence. A genome-wide sRNA study suggested that some sRNAs are linked to the antibiotic resistance and stress response in another Enteroccocus: E. faecium.
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Tabashnik, B. E., Brévault, T., Carrière, Y. "Insect resistance to Bt crops: lessons from the first billion acres." Nature biotechnology 31.6 (2013): 510-521. Since Cry6Aa proteins function differently than other Cry proteins, they are combined with other proteins to decrease the development of pest resistance. Recent studies suggest this protein functions better in combination with other virulence factors such as other Cry proteins and metalloproteinases.
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Whether chytridiomycosis is a new, emergent pathogen or a pathogen with recently increased virulence is unclear. The disease in its epizootic form was first discovered in 1993 in dead and dying frogs in Queensland, Australia. It had been present in the country since at least 1978 and is widespread across Australia. It is also found in Africa, the Americas, Europe, New Zealand, and Oceania.
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Finally, scientists are studying molecular genetics and genomics of the major pathogen, B. glumae, to understand the mechanism underlying its bacterial pathogenesis in rice. Genetic elements governing the production of virulence factors are being identified and characterized. Authors Jong Hyun Ham, Assistant Professor, Department of Plant Pathology & Crop Physiology, LSU AgCenter, Baton Rouge, La.; and Donald E. Groth, Florence Avalon Daggett Professor, Rice Research Station, Crowley, La.
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Changes in the normal, healthy vaginal microbiota is an indication of infections, such as candidiasis or bacterial vaginosis. Candida albicans inhibits the growth of Lactobacillus species, while Lactobacillus species which produce hydrogen peroxide inhibit the growth and virulence of Candida albicans in both the vagina and the gut. Fungal genera that have been detected in the vagina include Candida, Pichia, Eurotium, Alternaria, Rhodotorula, and Cladosporium, among others.
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The large genetic and phenotypic diversity of IBV have been resulting in common vaccination failures. In addition, new strains of IBV, not present in commercial vaccines, can cause the disease in IB vaccinated flocks. Attenuated vaccines will revert to virulence by consecutive passage in chickens in densely populated areas, and may reassort with field strains, generating potentially important variants. Definitive diagnosis relies on viral isolation and characterization.
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Adhesin expression is the suspected first mechanism by which C. glabrata forms fungal biofilms, proved to be more resistant to antifungals than the planktonic cells. C. glabrata genome frequently undergoes rearrangements that are hypothesized to contribute to the improvement of this yeast's fitness towards exposure to stressful conditions, and some authors consider that this property is connected to the virulence potential of this yeast.
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Helicobacter pylori is one of the major causative factors of peptic ulcer disease. It secretes urease to create an alkaline environment, which is suitable for its survival. It expresses blood group antigen adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as CagA and PicB, which cause stomach mucosal inflammation.
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An example of this difference is seen in the species' virulence. Only a few strains of S. aureus are associated with infections in humans. This demonstrates that there is a large range of infectious ability within the species. It has been proposed that one possible reason for the great deal of heterogeneity within the species could be due to its reliance on heterogeneous infections.
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Though S. aureus has quick reproductive and micro-evolutionary rates, there are multiple barriers that prevent evolution with the species. One such barrier is AGR, which is a global accessory gene regulator within the bacteria. This such regulator has been linked to the virulence level of the bacteria. Loss of function mutations within this gene have been found to increase the fitness of the bacterium containing it.
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F. solani rots the roots of its host plant. It also causes soft rot of plant tissues by penetrating plant cell walls and destroying the torus. It is implicated, along with Pythium myriotylum, in pod rot of the pods of groundnuts. Virulence of this agent in plants is controlled by the cutinase genes cut1 and cut2. These genes are upregulated by exposure to the plant’s cutin monomers.
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Additionally, by forming the fibrillar matrix, the YadA domain protects the bacteria by facilitating agglutination resistance, serum resistance, complement inactivation and phagocytosis resistance. The importance of adhesins to YadA function and Yersinia survival is huge. Attachment further allows more interactions and increase of biofilm formation to aid bacterial colonization. In Yersinia, it helps initiate the infectious process in host cells and are critical virulence factors.
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Peptidoglycan-N-acetylglucosamine deacetylase (, HP310, PgdA, SpPgdA, BC1960, peptidoglycan deacetylase, N-acetylglucosamine deacetylase, peptidoglycan GlcNAc deacetylase, peptidoglycan N-acetylglucosamine deacetylase, PG N-deacetylase) is an enzyme with systematic name peptidoglycan-N- acetylglucosamine amidohydrolase. This enzyme catalyses the following chemical reaction : peptidoglycan-N-acetyl-D-glucosamine + H2O \rightleftharpoons peptidoglycan-D-glucosamine + acetate This enzyme contributes to virulence of Helicobacter pylori, Listeria monocytogenes and Streptococcus suis.
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RTX toxins have been found in numerous strains of pathogenic E. coli. The prototypical RTX toxin, α-haemolysin (HlyA; TC# 1.C.11.1.3), is a common virulence factor in uropathogenic E. coli (UPEC), the leading cause of urinary tract infections. The hly operon encodes the RTX toxin (HlyA), the HlyA activation protein HlyC (an acyltransferase; TC# 9.A.40.1.1), and two proteins of the T1SS machinery.
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Dickeya spp. Furthermore, Dickeya solani is more aggressive in causing black leg than other species. Dickeya solani can induce disease at lower inoculum levels. One reason for this is that Dickeya solani produces more cell wall degrading enzymes when compared to other Dickeya spp. Dickeya spp. have virulence factors such as extracellular enzymes, type III secretion systems, and phospholipases (Zhou, et al., 2015). Dickeya spp.
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Fluorescein-labeled proaerolysin (FLAER) is used in a flow cytometric assay to diagnose paroxysmal nocturnal hemoglobinuria (PNH). The assay takes advantage of the action of proaerolysin, a prototoxin of aerolysin, a virulence factor of the bacterium Aeromonas hydrophila. Proaerolysin binds to the glycophosphatidylinositol(GPI) anchor in the plasma membrane of cells. Cells affected by PNH lack GPI anchoring proteins, and thus are not bound by proaerolysin.
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To enter the host the bacteria uses the pili to adhere to and penetrate mucosal surfaces. The pili are a necessary virulence factor for N. gonorrhoeae; without them, the bacterium is unable to cause infection. To move, individual bacteria use their pili like a grappling hook: first, they are extended from the cell surface and attach to a substrate. Subsequent pilus retraction drags the cell forward.
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Long-term culture of B. burgdorferi results in a loss of some plasmids and changes in expressed protein profiles. Associated with the loss of plasmids is a loss in the ability of the organism to infect laboratory animals, suggesting the plasmids encode key genes involved in virulence. Chemical analysis of the external membrane of B. burgdorferi revealed the presence of 46% proteins, 51% lipids and 3% carbohydrates.
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The change allows the virus to use the Asian tiger mosquito (an invasive species) as a vector in addition to the more strictly tropical main vector, Aedes aegypti. In July 2006, a team analyzed the virus' RNA and determined the genetic changes that have occurred in various strains of the virus and identified those genetic sequences which led to the increased virulence of recent strains.
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This system was shown to be a strong selective pressure for the acquisition of antibiotic resistance and virulence factor in bacterial pathogens. Therapies based on CRISPR–Cas3 gene editing technology delivered by engineered bacteriophages could be used to destroy targeted DNA in pathogens. Cas3 is more destructive than the better known Cas9. Research suggests that CRISPR is an effective way to limit replication of multiple herpesviruses.
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One of the key forces driving gene gain is thought to be horizontal (lateral) gene transfer (LGT). It is of particular interest in microbial studies because these mobile genetic elements may introduce virulence factors into a new genome. A comparative study conducted by Gill et al. in 2005 postulated that LGT may have been the cause for pathogen variations between Staphylococcus epidermidis and Staphylococcus aureus.
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Nosema ceranae was first described in 1996 and was identified as a disease of Apis mellifera in 2004 in Taiwan.(Huang et al., 2007; submitted in 2005 but published in 2007). Since its emergence in honeybees, N. ceranae has been identified in bumblebee species in South America, China, and England where infection studies indicate N. ceranae has a higher virulence in bumblebees than honeybees.
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Virus virulence factors allow it to replicate, modify host defenses, and spread within the host, and they are toxic to the host. They determine whether infection occurs and how severe the resulting viral disease symptoms are. Viruses often require receptor proteins on host cells to which they specifically bind. Typically, these host cell proteins are endocytosed and the bound virus then enters the host cell.
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Fungal, oomycete and nematode plant pathogens apparently express a few hundred effectors. So-called "core" effectors are defined operationally by their wide distribution across the population of a particular pathogen and their substantial contribution to pathogen virulence. Genomics can be used to identify core effectors, which can then be used to discover new R gene alleles, which can be used in plant breeding for disease resistance.
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Alpha- toxin has been shown to play a role in pathogenesis of disease, as hly knockout strains show reductions in invasiveness and virulence. The dosage of toxin can result in two different modes of activity. Low concentrations of toxin bind to specific, but unidentified, cell surface receptors and form the heptameric pores. This pore allows the exchange of monovalent ions, resulting in DNA fragmentation and eventually apoptosis.
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The response protects U. maydis from the host defense, and is necessary for the pathogen's virulence. Furthermore, U. maydis has a well- established recombinational DNA repair system which acts during mitosis and meiosis. The system may assist the pathogen in surviving DNA damage arising from the host plant's oxidative defensive response to infection. Cryptococcus neoformans is an encapsulated yeast that can live in both plants and animals.
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This process requires a gene called DMC1, which is a conserved homologue of genes recA in bacteria and RAD51 in eukaryotes, that mediates homologous chromosome pairing during meiosis and repair of DNA double-strand breaks. Thus, C.neoformans can undergo a meiosis, monokaryotic fruiting, that promotes recombinational repair in the oxidative, DNA damaging environment of the host macrophage, and the repair capability may contribute to its virulence.
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Transcriptional and post-transcriptional regulation of flagellar synthesis in C. jejuni enables proper biosynthesis of flagella and it is important for pathogenesis of this bacteria. Other important virulence factors of C. jejuni are the ability to produce N-linked glycosylation of more than 30 proteins. These proteins are important for the bacteria colonization, adherence and invasion. C. jejuni secretes Campylobacter invasive antigens (Cia) which facilitates the motility.
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E. histolytica may modulate the virulence of certain human viruses and is itself a host for its own viruses. For example, AIDS accentuates the damage and pathogenicity of E. histolytica. On the other hand, cells infected with HIV are often consumed by E. histolytica. Infective HIV remains viable within the amoeba, although there has been no proof of human reinfection from amoeba carrying this virus.
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A major study in F. t. novicida later demonstrated FtrA to be associated with a CRISPR/Cas system and to repress an endogenous transcript encoding a bacterial lipoprotein. FtrC (Francisella tularensis sRNA C) is the first sRNA shown to modulate the virulence capacity of F. tularensis. High expression of FtrC reduces intracellular multiplication of the bacteria in macrophages and in organs of infected mice.
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Age: Primary herpetic gingivostomatitis is common in children from 6 months to 5 years old. This virus is also common in young adults aged around 20–25. Immune system: The prevalence and severity of the disease is dependent on the host's immune response and the virulence of the virus. Environment: As this virus is very contagious it has the potential to spread quickly in enclosed environments e.g.
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TLR5 is expressed on both immune and non-immune cells. TLR5 recognizes bacterial flagellin, a principal component of bacterial flagella and a virulence factor. The activation of this receptor mobilizes the nuclear factor NF-κB and stimulates tumor necrosis factor-alpha production. TLR5 recognizes flagellin, which is the protein monomer that makes up the filament of bacterial flagella, found on nearly all motile bacteria.
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Said A. Ghabrial Said Amin (Gabe) Ghabrial (October 1, 1939 – November 26, 2018) was an Egyptian-American plant pathologist, known for his work on mycoviruses – viruses of fungi – and particularly their effects on the virulence of plant-pathogenic fungi. He also researched bean pod mottle virus, an economically important soybean disease. He was professor of plant pathology at the University of Kentucky (1986–2014).
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If they believe employers will increase wages as > their profits increase, then they believe the leopard can change his spots. > They should know that increased profits only increase the appetite for > profits. The desire for the accumulation of great wealth seems like a > disease, and disease has never been cured by increasing its virulence. > ...[T]he one lasting solution is the end of the profit system.
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A study by Chau et al. shows a negative correlation between acidogenicity of the biofilm and the fluoride release by GIC, suggestive that enough fluoride release may decrease the virulence of cariogenic biofilms. In addition, Ngo et al. (2006) studied the interaction between demineralised dentine and Fuji IX GP which includes a strontium – containing glass as opposed to the more conventional calcium-based glass in other GICs.
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MicF in E. coli was found to regulate the expression of a key structural gene that makes up the outer membrane of the E. coli cell. Shortly after, the Staphylococcus aureus sRNA RNAIII was found to act as a global regulator of S. aureus virulence and toxin secretion. Since these initial discoveries, over six thousand bacterial sRNAs have been identified, largely through RNA-sequencing experiments.
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Domestication typically involves about a decade of scientific research. Domesticating aquatic species involves fewer risks to humans than do land animals, which took a large toll in human lives. Most major human diseases originated in domesticated animals, including diseases such as smallpox and diphtheria, that like most infectious diseases, move to humans from animals. No human pathogens of comparable virulence have yet emerged from marine species.
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The pore-forming activity is not involved in causing the histone modifications. The alterations of the histones cause the down regulation of genes encoding proteins involved in the inflammatory response. Thus, LLO may be important in subverting the host immune response to L. monocytogenes. A PEST-like sequence is present in LLO and is considered essential for virulence, since mutants lacking the sequence lysed the host cell.
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The plague had a devastating effect on Europe's social structure; it induced people to live for the moment as illustrated by Giovanni Boccaccio in The Decameron (1353). It was a serious blow to the Roman Catholic Church and led to increased persecution of Jews, beggars, and lepers.National Geographic, 223. The plague is thought to have returned every generation with varying virulence and mortalities until the 18th century.
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The susceptibility to P. rettgeri is strongly tied to an allele of the antimicrobial peptide gene Diptericin. Surprisingly, the fly's defence against P. rettgeri seems to rely almost exclusively on Diptericin, as deletion of Diptericin leads to complete mortality. Meanwhile deletion of multiple other antimicrobial peptides has no effect on P. rettgeri virulence. Yet defence against P. burhodogranariea is determined by multiple antimicrobial peptides beyond just Diptericin.
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Large, broadly-based budding yeast cells characteristic of Blastomyces dermatitidis in a GMS-stained biopsy section from a human leg. Inhaled conidia of B. dermatitidis are phagocytosed by neutrophils and macrophages in alveoli. Some of these escape phagocytosis and transform into yeast phase rapidly. Having thick walls, these are resistant to phagocytosis and express glycoprotein, BAD-1, which is a virulence factor as well as an epitope.
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Mycoviruses of Botrytis cinerea. Botrytis cinerea not only infects plants, it also hosts several mycoviruses itself (see the table/image). A range of phenotypic alterations due to the mycoviral infection have been observed from symptomless to mild impact, or more severe phenotypic changes including reduction in pathogenicity, growth/suppression of mycelia, sporulation and sclerotia production, formation of abnormal colony sectors (Wu et al., 2010) and virulence.
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Cholera is rarely spread directly from person to person. V. cholerae also exists outside the human body in natural water sources, either by itself or through interacting with phytoplankton, zooplankton, or biotic and abiotic detritus. Drinking such water can also result in the disease, even without prior contamination through fecal matter. Selective pressures exist however in the aquatic environment that may reduce the virulence of V. cholerae.
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Brucella melitensis is a pathogenic bacterium that causes fever and inflammation of the epididymis in sheep and cattle and can be transmitted to humans through the consumption of unpasteurized milk. Malate synthase has been identified as a potential virulence factor in this bacterium. In 2016, Adi, et al. constructed a 3D crystalized structure of the protein to identify catalytic domains and investigate potential inhibitors.
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The wide variety of pathogenic and nonpathogenic strains that co-exist in aquatic environments are thought to allow for so many genetic varieties. Gene transfer is fairly common amongst bacteria, and recombination of different V. cholerae genes can lead to new virulent strains. A symbiotic relationship between V. cholerae and Ruminococcus obeum has been determined. R. obeum autoinducer represses the expression of several V. cholerae virulence factors.
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Pseudomonas aeruginosa is a known opportunistic pathogen. One of its virulence factors is its ability to produce pyocyanin, a toxin released to kill both microbes and mammalian cells alike. The pyocyanin production occurs when activated by PhoB. This implies that P. aeruginosa uses the low Pi as a signal that the host has been damaged and to start producing toxin to improve chances of its survival.
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It possesses a uniquely fusogenic type VI secretion system that is required for cell-cell spread and virulence in mammalian hosts. The bacterium also expresses a toxin called lethal factor 1. B. pseudomallei is one of the first Proteobacteria to be identified as containing an active type VI secretion system. It is also the only organism identified that contains up to six different type VI secretion systems.
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The Catabolite repression control (Crc) protein participates in suppressing expression of several genes involved in utilization of carbon sources in Pseudomonas bacteria. Presence of organic acids triggers activation of Crc and in conjunction with the Hfq protein genes that metabolize a given carbon source are downregulated until another more favorable carbon source is depleted. Crc-mediated regulation impact processes such as biofilm formation, virulence and antibiotic susceptibility.
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Elek's test or the Elek plate test is an in vitro test of virulence performed on specimens of Corynebacterium diphtheriae, the bacteria that causes diphtheria. It is used to test for toxigenicity of C. diphtheriae strains. The test uses immunodiffusion. A strip of filter paper impregnated with diphtheria antitoxin is buried just beneath the surface of a special agar plate before the agar hardens.
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The SraL RNA ('sra' for small RNA), also known as RyjA, is a small non-coding RNA discovered in E. coli, and later in Salmonella Tiphimurium. This ncRNA was found to be expressed only in stationary phase. It may possibly play a role in Salmonella virulence. The major stationary phase regulator RpoS is transcriptionally regulating SraL and directly binds to the sraL gene promoter.
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Parasite load is a measure of the number and virulence of the parasites that a host organism harbours. Quantitative parasitology deals with measures to quantify parasite loads in samples of hosts and to make statistical comparisons of parasitism across host samples. In evolutionary biology, parasite load has important implications for sexual selection and the evolution of sex, as well as openness to experience.Thornhill, Randy et al.
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Version: 20 August 1996.' URL Leaf chlorosis Symptoms of CTV infection are highly variable and depend on several factors including host, virulence of the particular virus strain, and environmental conditions. The three most common groupings of symptoms are decline (quick and slow), stem-pitting, and seedling yellows. Decline is generally exhibited with sweet orange, mandarin, or grapefruit when they are grafted on infected sour orange rootstock.
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The two plasmids are pTiC58, responsible for the processes involved in virulence, and pAtC58, dubbed the "cryptic" plasmid. The pAtC58 plasmid has been shown to be involved in the metabolism of opines and to conjugate with other bacteria in the absence of the pTiC58 plasmid. If the pTi plasmid is removed, the tumor growth that is the means of classifying this species of bacteria does not occur.
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CagA is a protein and virulence factor inserted by Helicobacter pylori into gastric epithelia. Once activated by SRC phosphorylation, CagA binds to SHP2, allosterically activating it. This leads to morphological changes, abnormal mitogenic signals and sustained activity can result in apoptosis of the host cell. Epidemiological studies have shown roles of cagA- positive H. pylori in the development of atrophic gastritis, peptic ulcer disease and gastric carcinoma.
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E. coli fimbriae EAEC is transmitted through the fecal-oral route and primarily contaminated by food and water. EAEC has been associated with many symptoms such as diarrhea in some individuals and intestinal colonization in others. Because many strains of EAEC have been identified, it is difficult to identify the mechanism of its pathogenesis. Most candidate virulence genes are not always connected with disease.
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In order for pathogenic bacteria to invade a cell, communication with the host cell is required. The first step for invading bacteria is usually adhesion to host cells. Strong anchoring, a characteristic that determines virulence, prevents the bacteria from being washed away before infection occurs. Bacterial cells can bind to many host cell surface structures such as glycolipids and glycoproteins which serve as attachment receptors.
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Resistance plasmids by definition carry one or more antibiotic resistance genes. They are frequently accompanied by the genes encoding virulence determinants, specific enzymes or resistance to toxic heavy metals. Multiple resistance genes are commonly arranged in the resistance cassettes. The antibiotic resistance genes found on the plasmids confer resistance to most of the antibiotic classes used nowadays, for example, beta-lactams, fluoroquinolones and aminoglycosides.
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Megabirnaviridae is a family of double-stranded RNA viruses with one genus Megabirnavirus which infects fungi. The group name derives from member's bipartite dsRNA genome and mega that is greater genome size (16 kbp) than families Birnaviridae (6 kbp) and Picobirnaviridae (4 kbp). There is only one species in this family: the type species Rosellinia necatrix megabirnavirus 1. Diseases associated with this family include: reduced host virulence.
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The best-known neuraminidase is the viral neuraminidase, a drug target for the prevention of the spread of influenza infection. The viral neuraminidases are frequently used as antigenic determinants found on the surface of the influenza virus. Some variants of the influenza neuraminidase confer more virulence to the virus than others. Other homologues are found in mammalian cells, which have a range of functions.
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In particular, it was intended to address virulence factors rather than structure and function of the pathogen cell wall according to the motto "targeting virulence: a new paradigm for antifungals". Moreover, he was interested in the development of new biological drugs such as plasmin as well as small molecules which are capable of influencing inflammation in the context of signal transduction such as sphingosine-1-phosphate. In addition, there now was a focus on small molecules modulating the function of human polymerase alpha which at a time modulates proliferation of keratinocytes and various viruses including human papilloma viruses (HPV), which is most relevant in the context of non-melanoma skin cancer treatment. Korting was the recipient of several scientific awards, including the Paul Gerson Unna Prize from the German Dermatological Society as well as the prize for promotion of research of Deutschsprachige Mykologische Gesellschaft.
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In molecular biology, the protein domain YopE refers to the secretion of virulence factors in Gram-negative bacteria involves transportation of the protein across two membranes to reach the cell exterior. It not only infects the host cell but also protects the bacteria. It undergoes several mechanisms to evade the host's immune system. This particular protein domain can be referred to as a Rho GTPase-activating protein (GAP).
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TAAs also go by another name, oligomeric coiled-coil adhesins, which is shortened to OCAs. In essence, they are virulence factors, factors that make the bacteria harmful and infective to the host organism. TAAs are just one of many methods bacteria use to infect their hosts, infection resulting in diseases such as pneumonia, sepsis, and meningitis. Most bacteria infect their host through a method named the secretion pathway.
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Exotoxins such as PVL constitute essential components of the virulence mechanisms of S. aureus. Nearly all strains secrete lethal factors that convert host tissues into nutrients required for bacterial growth. PVL is a member of the synergohymenotropic toxin family that induces pores in the membranes of cells. The PVL factor is encoded in a prophage-- designated as Φ-PVL--which is a virus integrated into the S. aureus bacterial chromosome.
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Advances in genotyping methods have led to improved genetic analysis for variation and relatedness. These methods include multiple-locus variable-number tandem repeat analysis (MLVA) and typing systems using canonical single-nucleotide polymorphisms. The Ames ancestor chromosome was sequenced in 2003 and contributes to the identification of genes involved in the virulence of B. anthracis. Recently, B. anthracis isolate H9401 was isolated from a Korean patient suffering from gastrointestinal anthrax.
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These proteins have either an EAL or an HD-GYP amino acid motif. Processes that are known to be regulated by cyclic di-GMP, at least in some organisms, include biofilm formation, motility and virulence factor production. Cyclic di-GMP levels are regulated using a variety of mechanisms. Many proteins with GGDEF, EAL or HD-GYP domains are found with other domains that can receive signals, such as PAS domains.
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Aureolysin cleaves various immune components and host proteins. It is important for hiding the bacterium from the immune system and is responsible for mediating the transition of a biofilm forming phenotype to a mobile and invasive one. There are many different targets of aureolysin and the effect on each is critical for the bacterium's virulence. One major way aureolysin contributes to infection, is by inactivating certain targets within the complement system.
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As hosts and parasites evolve together, their relationships often change. When a parasite is in a sole relationship with a host, selection drives the relationship to become more benign, even mutualistic, as the parasite can reproduce for longer if its host lives longer. But where parasites are competing, selection favours the parasite that reproduces fastest, leading to increased virulence. There are thus varied possibilities in host–parasite coevolution.
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This process constitutes an effective cell-cell signaling mechanism via membrane vesicle trafficking from secretory cell to the target cells in human or animal body. Recently, the process has been extended to host-pathogen interface, wherein, gram negative microbes secrete bacterial outer membrane vesicles containing fully conformed signal proteins and virulence factors via exocytosis of nano- sized vesicles, in order to control host or target cell activities and exploit their environment.
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Helicobacter pylori colonizes the human stomach and duodenum. In some cases it can cause stomach cancer and MALT lymphoma. Animal models have demonstrated Koch's third and fourth postulates for the role of Helicobacter pylori in the causation of stomach cancer. The mechanism by which H. pylori causes cancer may involve chronic inflammation, or the direct action of some of its virulence factors, for example, CagA has been implicated in carcinogenesis.
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Helicobacter pylori infection is an essential risk factor in 65–80% of gastric cancers, but only 2% of people with Helicobacter infections develop stomach cancer. The mechanism by which H. pylori induces stomach cancer potentially involves chronic inflammation, or the action of H. pylori virulence factors such as CagA. It was estimated that Epstein–Barr virus is responsible for 84,000 cases per year. AIDS is also associated with elevated risk.
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However, evidence of horizontal genetic transfer has also been reported. The first pivotal step in infectious pathogenesis is the attachment to the host tissues. The M-protein, the most extensively studied Streptococcus dysgalactiae subspecies equisimilis virulence factor, has been documented to facilitate both adherence to and internalization into host cells. Other adhesins have also been described, including the genes gfba, fnB, fbBA, fnBB, lmb and gapC; all mediating binding to fibronectin.
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Lastly, binding by sIgA can downregulate the expression of virulence factors e.g. involved in adhesion or nutrient acquisition by commensal bacteria. If the homeostasis breaks down, innate immune responses directed against commensal enteric bacteria lead to a shift in the species composition (dysbiosis). Invasive species are better equipped to resist or take advantage of host inflammatory mechanisms and in the perturbed niche successfully compete with the resident microbiota.
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Indole is an aromatic heterocyclic organic compound with formula C8H7N. It has a bicyclic structure, consisting of a six-membered benzene ring fused to a five-membered pyrrole ring. Indole is widely distributed in the natural environment and can be produced by a variety of bacteria. As an intercellular signal molecule, indole regulates various aspects of bacterial physiology, including spore formation, plasmid stability, resistance to drugs, biofilm formation, and virulence.
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Pseudomonas syringae isolates carry a range of virulence factors called type III secretion system (T3SS) effector proteins. These proteins primarily function to cause disease symptoms and manipulate the host's immune response to facilitate infection. The major family of T3SS effectors in P. syringae is the hrp gene cluster, coding for the Hrp secretion apparatus. The pathogens also produce phytotoxins which injure the plant and can suppress the host immune system.
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In prokaryotes, a similar protein complex transports polypeptides across the (inner) plasma membrane or integrates membrane proteins. Bacterial pathogens can also assemble other translocons in their host membranes, allowing them to export virulence factors into their target cells. In either case, the protein complex are formed from Sec proteins (Sec: secretory), with the hetrotrimeric Sec61 being the channel. In prokaryotes, the homologous channel complex is known as SecYEG.
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Filamentous cells share many similarities with yeast cells. Both cell types seem to play a specific, distinctive role in the survival and pathogenicity of C. albicans. Yeast cells seem to be better suited for the dissemination in the bloodstream while hyphal cells have been proposed as a virulence factor. Hyphal cells are invasive and speculated to be important for tissue penetration, colonization of organs and surviving plus escaping macrophages.
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Research suggests that high water temperatures can be indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off.
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However, research is successfully identifying the quantity and type of plant resistance molecules that are produced in response to pathogen associated molecular patterns (PAMPs), and their effects on the activity and virulence of pathogens such as P. atrosepticum.Kroener A, Hamelin G, Andrivon D, Val F, Umr Igepp I. 2011. Quantitative Resistance of Potato to Pectobacterium Atrosepticum and Phytophthora Infestans: Integrating PAMP- Triggered Response and Pathogen Growth. PLoS One 6:23331.
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H.1969 N.Z.Entomologist, Volume 4(2), 1969Treat, Asher Eugene (1975) Mites of Moths and Butterflies. Comstock Pub. Assoc. They are notable in that only one ear is ever colonised, leaving one intact so that the host is still able to detect the sound from hunting bats. This is taken to be an adaptation reducing the 'virulence' of the parasite to prevent its host's destruction, and therefore its own.
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Adhesins are cell-surface components or appendages of bacteria that facilitate adhesion or adherence to other cells or to surfaces, usually in the host they are infecting or living in. Adhesins are a type of virulence factor. Adherence is an essential step in bacterial pathogenesis or infection, required for colonizing a new host. Adhesion and bacterial adhesins are also a potential target for prophylaxis or treatment of bacterial infections.
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In situations such as these, we would expect there to be selection for cooperation amongst the viruses in a group in such a way that the group will not "kill the rabbit too early". It is of course true that any group behavior is the result of individual traits, such as individual viruses suppressing the virulence of their neighbours, but the causes of phenotypes are rarely the causes of fitness differences.
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As an inhibitory cytokine, IL-10 facilitates the infection of human alveolar macrophages and monocytes by completely reversing the protective effect of IFNγ against intracellular Legionella pneumophila replication. Yersinia enterocolitica has also been shown to releases virulence antigen LcrV, which induces IL-10 through Toll-like receptor-2 and CD14 (an accessory surface protein of TLR4-mediated LPS-signaling), resulting in the suppression of IFNγ and TNF-alpha suppression.
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Two virus-free isolates were successfully infected by purified TmPV1 using protoplast transfection. Mice challenged with TmPV1-infected T. marneffei isolates showed significantly shortened survival time and higher fungal burden in organs than mice challenged with isogenic TmPV1-free isolates. Transcriptomic analysis showed that TmPV1 causes aberrant expression of various genes in T. marneffei, with upregulation of potential virulence factors and suppression of RNA interference (RNAi)-related genes.
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Additionally, regulatory genes outside of the PAI may regulate virulence genes in the pathogenicity island. Regulation genes typically encoded on PAIs include AraC-like proteins and two-component response regulators. PAIs can be considered unstable DNA regions as they are susceptible to deletions or mobilization. This may be due to the structure of PAIs, with direct repeats, insertion sequences and association with tRNA that enables deletion and mobilization at higher frequencies.
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The induced behavioral change in the host thus leads to the parasite's increased success in completing its life cycle. In general, whether a specific behavioral change serves an adaptive purpose for the parasite, the host, or both, depends on the entire "host-parasite system": The life cycle of the pathogen, its virulence and the host's immune response. Conversely, evolved behaviors of the host may be a result of adaptations to parasitism.
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Salmonella that can express only one "H" antigen phase consequently have motile and non-motile phenotypes and are termed monophasic, whilst isolates that lack any "H" antigen expression are termed non-motile. Pathogenic strains of Salmonella Typhi, Salmonella Paratyphi C, and Salmonella Dublin carry the capsular "Vi" antigen (Vi for virulence), which is a special subtype of the capsule's K antigen (from the German word Kapsel meaning capsule).
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Loussert, C., Schmitt, C., Prevost, M.C., Balloy, V., Fadel, E., Philippe, B., Kauffmann-Lacroix, C., Latge, J.P., and Beauvais, A. (2010). In vivo biofilm composition of Aspergillus fumigatus. Cell Microbiol 12, 405-410 Besides its role in fungal virulence, certain fractions of laboratory purified galactosaminogalactan has been shown to induce neutrophil apoptosis Robinet, P., Baychelier, F., Fontaine, T., Picard, C., Debre, P., Vieillard, V., Latge, J.P., and Elbim, C. (2014).
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In the liver a similar pathological sequence ensues, leading to amebic liver abscesses. The trophozoites can also end up in other organs, sometimes via the bloodstream, sometimes via liver abscess rupture or fistulas. In all locations, similar pathology can occur. Transcriptomic study of E. histolytica for promoter analysis of variable expression class of all the genes reveals that the highly transcribed genes of E. histolytica belongs to virulence factor genes.
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Several Fusarium species provide useful model systems for research in molecular biology. Considering F. sporotrichioides specifically, sequences of known genes of the species have been used to study potential virulence genes in other fusaria, for example in the characterisation of the trichodiene synthase gene in F. graminearum. Moreover, the generation of F. sporotrichioides mutant libraries has been a particularly useful approach to studying the phytotoxicity of the fusaria.
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The vector is then turned into the desired strain with the help of the virulence genes of the bacterium. It is then transferred and integrated into the genomic DNA of the host plant by non-homologous recombination at random sites. This method has a low yield and is a slow process, and it is the most effective when used with dicotyledonous plants such as, tomato, potato, and tobacco.
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S. aureus delta toxin is encoded for by the hld gene. The hld gene, of which the 3’ end encodes for delta toxin, is involved in the accessory gene regulator (agr) system. This system controls the signaling and creation of cell-associated and secreted virulence factors. Delta toxin is also secreted from S. aureus without a signal peptide, but the toxin itself has been speculated to make an effective signal peptide.
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The GBS capsule is probably the key virulence factor because it helps GBS escape from the host defence mechanisms interfering with phagocytic killing of GBS by human phagocytes. The GBS β-haemolysin is considered almost identical to the GBS pigment (granadaene). GBS was recognized as a pathogen in cattle by Edmond Nocard and Mollereau in the late 1880s. It can cause bovine mastitis (inflammation of the udder) in dairy cows.
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Serine-arginine family of RNA-binding protein Slr1 was found exert control on the polarized growth in Candida albicans. Slr1 mutations in mice results in decreased filamentation and reduces damage to epithelial and endothelial cells that leads to extended survival rate compared to the Slr1 wild-type strains. Therefore, this research reveals that SR-like protein Slr1 plays a role in instigating the hyphal formation and virulence in C. albicans.
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These phenazine natural products have been implicated in the virulence and competitive fitness of producing organisms. For example, the phenazine pyocyanin produced by Pseudomonas aeruginosa contributes to its ability to colonise the lungs of cystic fibrosis patients. Similarly, phenazine-1-carboxylic acid, produced by a number of Pseudomonas, increases survival in soil environments and has been shown to be essential for the biological control activity of certain strains.
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Septicaemia eventually develops and the bacteria become localized in epithelial cells and macrophages of most organs, conjunctiva, and gastrointestinal tracts. It can also be passed in the eggs. Stress will commonly trigger onset of severe symptoms, resulting in rapid deterioration and death. C. psittaci strains are similar in virulence, grow readily in cell culture, have 16S rRNA genes that differ by <0.8%, and belong to eight known serotypes.
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Staphyloxanthin is a carotenoid pigment that is produced by some strains of Staphylococcus aureus, and is responsible for the characteristic golden color that gives S. aureus its species name. Staphyloxanthin also acts as a virulence factor. It has an antioxidant action that helps the microbe evade death by reactive oxygen species produced by the host immune system. The pigment staphyloxanthin gave the bacteria Staphylococcus aureus a yellow color.
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Raoultella terrigena is a Gram-negative bacterial species of the genus Raoultella, previously classified in the genus Klebsiella. It has primarily been isolated from soil and water samples, but rarely from humans. Studies have estimated fewer than 1% of healthy people harbor this species. This species has shown no connection with disease in humans despite expressing many of the virulence factors expressed by other Klebsiella species such as Klebsiella pneumoniae.
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PyoverdinesFor the purposes of this page, pyoverdine will generally refer (unless otherwise noted) to the pyoverdine produced by Pseudomonas aeruginosa strain PAO1. It has been subjected to the most extensive study and can be considered the prototypical siderophore. (alternatively, and less commonly, spelled as pyoverdins) are fluorescent siderophores produced by certain pseudomonads. Pyoverdines are important virulence factors, and are required for pathogenesis in many biological models of infection.
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The Black Death was so devastating that a comparable plague in terms of virulence had not been seen since the Justinian plague, before the Medieval warm period. This gap in plague activity during the Medieval Warm Period contributes to the hypothesis that climate conditions would have affected Europe's susceptibility to disease when the climate began to cool during the arrival of the Little Ice Age in the 13th century.
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But bear in > mind that many — if not all — of the people tearing down Clinton and her new > memoir, What Happened, haven't actually read it. Bear in mind, too, that few > — if any — of these same people called out Bernie Sanders for writing his > own campaign memoir, one that dropped just days post-election. No, there's > some sort of special virulence reserved for Clinton. And she gets it.
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Activation of NLRP1B-dependent inflammasome responses appears in host defense with mechanism like IL-1β and neutrophils. NLRP1B can function as a sensor of bacterial proteases, immune responses are specifically activated by virulence factors. It is not clear what stimuli might activate NLRP1A, the other known functional murine NLRP1 paralog. The study identified a mouse carrying a missense gain-of-function mutation in NLRP1A (Q593P) that active inflammasome responses.
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Plaque hypotheses are theories to explain the role of plaque bacteria in dental caries and in periodontitis. They rely heavily on the postulates of Koch (formulated in 1884) and on the work of Louis Pasteur (1822-1895). Changing perceptions have altered treatment models. The hypotheses have sought to establish both in caries and in periodontitis a relation between pathogen virulence, environmental considerations, plaque biofilm structure and the host response.
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These plant pathogen genomes have been growing larger over the years due to repeat-driven expansion. The repeat-rich regions contain genes coding for host interaction proteins. With the addition of more and more repeats to these regions the plants increase the possibility of developing new virulence factors through mutation and other forms of genetic recombination. In this way it is beneficial for these plant pathogens to have larger genomes.
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Franz attempts to use copper in the same way as biological systems to target antimicrobial agents. She has looked at iron and copper as ionophores; which are important in the virulence of Cryptococcus neoformans. Franz also works on anti-cancer prochelators; molecules that do not have much affinity for metal ions, but can be triggered until they undergo a chemical conversion. Cancer cells have different metallomes than normal cells.
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Motility is a key virulence determinant in Pseudomonas aeruginosa. Pseudomonas aeruginosa has three distinct methods of moving across or through a medium. Rhamnolipids are particularly important in swarming motility where they are postulated to lower the surface tension of the surface through their surfactant properties, allowing the bacterial cell to swarm. New evidence suggests that rhamnolipids are necessary to allow Pseudomonas aeruginosa cells to overcome attachment mediated by type IV pili.
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Finlay's lab is based in Vancouver, British Columbia, Canada in the Michael Smith Laboratories at the University of British Columbia, and involves a multidisciplinary research program exploring how microbes contribute to both human health and disease. The lab specifically focuses on type III secreted virulence factors from Salmonella and pathogenic E. coli, how microbiota influence infectious diarrhea outcomes, and the role of the microbiota in asthma, malnutrition, and environmental enteropathy.
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A book from the 1980s listed the pathogenic yeasts of candidiasis in probable descending order of virulence for humans as: C. albicans, C. tropicalis, C. stellatoidea, C. glabrata, C. krusei, C. parapsilosis, C. guilliermondii, C. viswanathii, C. lusitaniae, and Rhodotorula mucilaginosa. Candida glabrata is the second most common Candida pathogen after C. albicans, causing infections of the urogenital tract, and of the bloodstream (candidemia). C. auris has been more recently identified.
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As well as genes that produce toxins, other genes have been identified which help S. scabies to infect plants. A tomatinase enzyme, encoded by tomA which can degrade the antimicrobial saponin α–tomatine. The aerial growth of mutants lacking the gene is inhibited, but the mycelium is able to continue to grow. Nec1 is another protein that is required for virulence, which is secreted out of the bacteria.
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Pathogenic Vibrio species can cause foodborne illness (infection), usually associated with eating undercooked seafood. The pathogenic features can be linked to quorum sensing, where bacteria are able to express their virulence factor via their signalling molecules. V. vulnificus outbreaks commonly occur in warm climates and small, generally lethal, outbreaks occur regularly. An outbreak occurred in New Orleans after Hurricane Katrina, and several lethal cases occur most years in Florida.
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Candidalysin is a cytolytic 31-amino acid α-helical amphipathic peptide toxin found in the opportunistic pathogen Candida albicans that activates epithelial cells. As such, Candidalysin is a rare fungal example of a classical virulence factor. Hyphal morphogenesis in C. albicans is associated with damage to host epithelial cells; during this process Candidalysin is released. Candidalysin promotes damage of oral epithelial cells by inducing lactate dehydrogenase release and calcium ion influx.
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The latter causes tetanus and is vaccinated against by the DTaP vaccine. Botulin is produced by Clostridium botulinum and causes the deadly disease botulism. While patients may sometimes complain of side effects after a vaccine, these are associated with the process of mounting an immune response and clearing the toxoid, not the direct effects of the toxoid. The toxoid does not have virulence as the toxin did before inactivation.
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Fungi from the genus Coelomomyces (order Blastocladiales) develop inside the visceral cavity of mosquito larvae. The species Coelomomyces stegomyiae was first found on the Asian tiger mosquito. Paramecia, or ciliates, can also affect Ae. albopictus larvae, and the first detected species was Lambornella stegomyiae (Hymenostomatida: Tetrahymenidae). The virulence, mortality rate, and subsequent possibilities of Lambornella being implemented as a biological remedy to control Ae. albopictus, however, has conflicting views.
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For example, YopN and TyeA are positioned as a plug on the apparatus so only their conformational change, induced by their interaction with certain host cell membrane proteins, will cause the unblocking of the secretory pathway. Secretion is regulated in this fashion so that proteins are not expelled into the extracellular matrix and elicit an immune response. Since this pathway gives secretion selectivity, it is a virulence factor.
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Fifteen different serotype variants (serovars) have been recognized for A. pleuropneumoniae, based on the different capsular polysaccharides exhibited. Two different biovars exist, with biovar 1 having 13 different serovars and biovar 2 having two serovars. Differences in virulence potential, immunogenicity, and worldwide geographical distribution contribute to the diversity of the A. pleuropneumoniae serotypes. All 15 serotypes can cause disease, with one serotype usually predominating in a particular herd.
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Stress commonly triggers onset of severe symptoms, resulting in rapid deterioration and death. C. psittaci strains are similar in virulence, grow readily in cell culture, have 16S-rRNA genes that differ by <0.8%, and belong to eight known serovars. All should be considered to be readily transmissible to humans. C. psittaci serovar A is endemic among psittacine birds and has caused sporadic zoonotic disease in humans, other mammals, and tortoises.
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Bacterial secretion systems are protein complexes present on the cell membranes of bacteria for secretion of substances. Specifically, they are the cellular devices used by pathogenic bacteria to secrete their virulence factors (mainly of proteins) to invade the host cells. They can be classified into different types based on their specific structure, composition and activity. These major differences can be distinguished between Gram-negative and Gram-positive bacteria.
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Ribbon diagram of the Cif dimer from P. aeruginosa PA14. From . The CFTR inhibitory factor (Cif) is a protein virulence factor secreted by the Gram- negative bacteria Pseudomonas aeruginosa and Acinetobacter nosocomialis. Discovered at Dartmouth Medical School, Cif is able to alter the trafficking of select ABC transporters in eukaryotic epithelial cells, such as the cystic fibrosis transmembrane conductance regulator (CFTR), and P-glycoprotein by interfering with the host deubiquitinating machinery.
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Primary pathogens cause disease as a result of their presence or activity within the normal, healthy host, and their intrinsic virulence (the severity of the disease they cause) is, in part, a necessary consequence of their need to reproduce and spread. Many of the most common primary pathogens of humans only infect humans, however, many serious diseases are caused by organisms acquired from the environment or that infect non-human hosts.
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Harper M, Cox AD, St Michael F, Wilkie IW, Boyce JD, Adler B. A heptosyltransferase mutant of Pasteurella multocida produces a truncated lipopolysaccharide structure and is attenuated in virulence. Infect. Immun. 2004; 72(6):3436-43. Strains that cause atrophic rhinitis in pigs are unique as they also have P. multocida toxin (PMT) residing on a bacteriophage. PMT is responsible for the twisted snouts observed in pigs infected with the bacteria.
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Nizet's laboratory applies molecular genetic approaches to discover and characterize bacterial virulence factors involved in host cell injury, epithelial adherence, cellular invasion, inflammation, molecular mimicry and resistance to immunologic clearance. The group focuses on the function of host phagocytic cells, such as macrophages and neutrophils, to understand the contribution of host factors such as antimicrobial peptides, leukocyte surface receptors, signal transduction pathways, and transcription factors in defense against invasive bacterial infection. Using this new information, therapeutic strategies for serious or antibiotic-resistant infections are pursued including neutralization of bacterial virulence phenotypes, pharmacologic augmentation of host phagocyte function, and repurposing of existing drugs for unexpected beneficial activities operating at the host-pathogen interface. Dr. Nizet's other longstanding academic focus areas include cross-disciplinary research and educational program development, enhancing graduate and postdoctoral training in biological, medical and pharmaceutical sciences, junior faculty development, encouragement of academic-industry collaborations, and public engagement in the sciences.
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In the microbial world, a relationship of predation can be established similar to that observed in the animal world. Considered, it has been seen that E. coli is the prey of multiple generalist predators, such as Myxococcus xanthus. In this predator-prey relationship, a parallel evolution of both species is observed through genomic and phenotypic modifications, in the case of E. coli the modifications are modified in two aspects involved in their virulence such as mucoid production (excessive production of exoplasmic acid alginate ) and the suppression of the OmpT gene, producing in future generations a better adaptation of one of the species that is counteracted by the evolution of the other, following a co-evolutionary model demonstrated by the Red Queen hypothesis.Nair, Ramith R.; Vasse, Marie; Wielgoss, Sébastien; Sun, Lei; Yu, Yuen-Tsu N.; Velicer, Gregory J. "Bacterial predator-prey coevolution accelerates genome evolution and selects on virulence-associated prey defences", Nature Communications, 2019, 10:4301.
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ADE can be induced when the strength of antibody-antigen interaction is below the certain threshold. This phenomenon might lead to both increased virus infectivity and virulence. The viruses that can cause ADE frequently share some common features such as antigenic diversity, abilities to replicate and establish persistence in immune cells. ADE can occur during the development of a primary or secondary viral infection, as well as after vaccination with a subsequent virus challenge.
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Although the ancestral function of the T6SS appears to be targeting of bacteria, a handful of systems have been identified that have evolved to target eukaryotic cells. In general, these eukaryote-targeting systems are involved in causing disease. For example, the intracellular pathogen Francisella tularensis requires the activity of a T6SS to escape from phagosomes and replicate in the cytoplasm of macrophages. The mechanism by which secreted proteins facilitate F. tularensis virulence is still unknown.
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Horizontal transmission is the transmission of organisms between biotic and/or abiotic members of an ecosystem that are not in a parent-progeny relationship. This concept has been generalized to include transmissions of infectious agents, symbionts, and cultural traits between humans. Because the evolutionary fate of the agent is not tied to reproductive success of the host, horizontal transmission tends to evolve virulence. It is therefore a critical concept for evolutionary medicine.
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The Type IV Secretion System (T4SS) is found in many species of Gram-negative and Gram-positive bacteria as well as in archea and are typically associated with conjugation or delivery of virulence proteins to eukaryotic cells. Some species of plant pathogen Xanthomonas, however, possess a particular T4SS capable of mediating CDI by delivering a peptidoglycan hydrolase. This effector kills targets that do not have the cognate immunity protein similar to other CDI systems.
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Invasion does elicit a host response ranging from mild to severe. Acid proteinases (proteases), elastase, keratinases, and other proteinases reportedly act as virulence factors. Additionally, the products of these degradative enzymes serve as nutrients for the fungi. The development of cell-mediated immunity correlated with delayed hypersensitivity and an inflammatory response is associated with clinical cure, whereas the lack of or a defective cell-mediated immunity predisposes the host to chronic or recurrent dermatophyte infection.
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Aureolysin (, protease III, staphylococcal metalloprotease, Staphylococcus aureus neutral proteinase) is an extracellular metalloprotease expressed by Staphylococcus aureus. This protease is a major contributor to the bacterium's virulence, or ability to cause disease, by cleaving host factors of the innate immune system as well as regulating S. aureus secreted toxins and cell wall proteins. To catalyze its enzymatic activities, aureolysin requires zinc and calcium which it obtains from the extracellular environment within the host.
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When inserted into liposomes and synthetic bilayers at low concentrations (2 nM), it provokes a cation-selective ion current with large unitary conductance. Chloride is not transported. It has been hypothesized that such channels could allow nutrient release and/or delivery of virulence factors during bacterial colonization of host plants. The leucine-zipper-like motifs may take part in the formation of oligomeric aggregates, and oligomerization could be related to HR elicitation.
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The journal scope of PLOS Pathogens is to feature PLOS Pathogens publishes original research and commentary that significantly advance the understanding of pathogens and how they interact with their host organisms. Topics include (but are not limited to) adaptive and innate immune defenses as well as pathogen countermeasures, emerging pathogens, evolution, genomics and gene regulation, model host organisms, pathogen-cell biology, pathogenesis, prions, proteomics and signal transduction, rational vaccine design, structural biology, and virulence factors.
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Hha, along with the chromatin-associated protein H-NS, is involved in the regulation of expression of the toxin alpha-haemolysin in response to osmolarity and temperature. YmoA modulates the expression of various virulence factors, such as Yop proteins and YadA adhesin, in response to temperature. RmoA is a plasmid R100 modulator involved in plasmid transfer. The HHA family of proteins display striking similarity to the oligomerisation domain of the H-NS proteins.
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Histopathology of Schistosoma haematobium eggs within the lining of the bladder.Certain bacterial infections also increase the risk of cancer, as seen in Helicobacter pylori-induced gastric carcinoma. The mechanism by which H. pylori causes cancer may involve chronic inflammation or the direct action of some of the bacteria's virulence factors. Parasitic infections strongly associated with cancer include Schistosoma haematobium (squamous cell carcinoma of the bladder) and the liver flukes, Opisthorchis viverrini and Clonorchis sinensis (cholangiocarcinoma).
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Hofstad T. Virulence determinants in non-spore-forming anaerobic bacteria. Scand J Infect Dis 1989; (Suppl.62):15–24. The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.
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Aspergillus fumigatus can survive on a variety of different nitrogen sources, and the assimilation of nitrogen is of clinical importance, as it has been shown to affect virulence. Proteins involved in nitrogen assimilation are transcriptionally regulated by the AfareA gene in A. fumigatus. Targeted mutation of the afareA gene showed a decrease in onset of mortality in a mouse model of invasion. The Ras regulated protein RhbA has also been implicated in nitrogen assimilation.
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Several different typing systems for Streptococcus dysgalactiae have been used, the majority originally devised for the closely related species Streptococcus pyogenes. The most widely employed method is emm-typing. The emm-gene encodes the M-protein, a major virulence factor in both S. pyogenes and Streptococcus dysgalactiae. It is ubiquitous in Streptococcus dysgalactiae subspecies equisimilis of human origin, and its hypervariability in the 5’-terminal region forms the basis for categorization into separate emm-types.
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Streptococcus zooepidemicus is a Lancefield group C streptococcus that was first isolated in 1934 by P. R. Edwards, and named Animal pyogens A. It's a mucosal commensal and opportunistic pathogen that infects several animals and humans, but most commonly isolated from the uterus of mares. It's a subspecies of Streptococcus equi, a contagious upper respiratory tract infection of horses, and shares greater than 98% DNA homology, as well as many of the same virulence factors.
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Outside the body, Listeria has flagellar-driven motility, sometimes described as a "tumbling motility". However, at 37 °C, flagella cease to develop and the bacterium instead usurps the host cell's cytoskeleton to move. Listeria, inventively, polymerizes an actin tail or "comet", from actin monomers in the host's cytoplasm with the promotion of virulence factor ActA. The comet forms in a polar manner and aids the bacterial migration to the host cell's outer membrane.
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A phyogenic non- motile Gram-positive cocci which forms into grape like clusters. Just like other forms of staph, S. aureus has a variety of virulence factors which include surface proteins involved in adherence, secretion of enzymes that degrade proteins, and secrete toxins which damage the host's cells. S. aureus expresses surface receptors for fibrinogen, fibronectin, and vitronectin. These surface receptors allow a bridge to be formed which binds to host endothelial cells.
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Severe acute respiratory syndrome (SARS) is caused by a new type of coronavirus.Mahy, (b) p. 459 Other coronaviruses were known to cause mild infections in humans, so the virulence and rapid spread of this novel virus strain caused alarm among health professionals as well as public fear. The fears of a major pandemic were not realised, and by July 2003, after causing around 8,000 cases and 800 deaths, the outbreak had ended.
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Overlapping activity with the other proteases, plus the complexity of virulence determinants and the infection site environment makes it difficult to determine the impact of the protease in pathogenesis. The elastinolytic properties of the protease could assist in spread of bacteria and also symptomatically to connective tissue destruction. Staphopain A participates in S. aureus self-regulatory events, by altering the phenotype of the bacteria via cleavage of surface proteins and by preventing biofilm formation.
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S. schenckii synthesizes melanin both in vitro and in vivo Melanin production is a virulence factor found in many fungi that cause disease and its production in S. schenckii protects the fungus from oxidative stress as well as ultraviolet light and macrophage killing. Melanin has been shown to be synthesized using the 1,8-DHN pentaketide pathway (below). Structures of some intermediates in the pentaketide pathway of melanin biosynthesis in S. schenckii. Adapted from.
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Multiple genetic elements of human-affecting pathogens contribute to the transfer of virulence factors: plasmids, pathogenicity island, prophages, bacteriophages, transposons, and integrative and conjugative elements. Pathogenicity islands and their detection are the focus of several bioinformatics efforts involved in pathogenomics. It is a common belief that "environmental bacterial strains" lack the capacity to harm or do damage to humans. However, recent studies show that bacteria from aquatic environments have acquired pathogenic strains through evolution.
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It has also allowed researchers to better understand genome evolution events - gene loss, gain, duplication, rearrangement - and how those events impact pathogen resistance and ability to cause disease. This influx of information has created a need for making the vast amounts of data accessible to researchers in the form of databases, and it has raised ethical questions about the wisdom of reconstructing previously extinct and deadly pathogens in order to better understand virulence.
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It is not fully understood how the genetic differences between M. africanum and M. tuberculosis give rise to the lower pathogenicity of the former. However, it is known that the Region of Difference 9 (RD9) is lacking in M. africanum but present in M. tuberculosis. M. africanum also has notable differences in lipid catabolism and metabolism. Additionally, virulence pathways such as the dosR/Rv0081 regulon or ESAT-6 regulation are disrupted in M. africanum.
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Lactuca serriola is the wild progenitor of cultivated lettuce (Lactuca sativa), and can be affected by lettuce downy mildew, one of the most serious diseases of lettuce. L. serriola has shown resistance to the plant pathogen Bremia lactucae, the cause of the disease. This pathogen is able to undergo sexual reproduction, and once virulent strains have been produced, can undergo rapid asexual reproductive cycles. As a result, there are many strains, which vary in virulence.
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Bifunctional hemolysin/adenylate cyclase is a protein that in B. pertussis (the bacteria that causes whooping cough) is encoded by the cyaA gene. This protein in turn is cleaved into a calmodulin-sensitive adenylate cyclase (cyaA–ACD) and hemolysin. Both are virulence factors facilitating respiratory tract colonization by B. pertussis. The cyaA–ACD binds to a M2 integrin cell surface receptor and inserts its N-terminal adenylyl cyclase domain into the cytosol.
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Bacteria produce various adhesins including lipoteichoic acid, trimeric autotransporter adhesins and a wide variety of other surface proteins to attach to host tissue. Capsules, made of carbohydrate, form part of the outer structure of many bacterial cells including Neisseria meningitidis. Capsules play important roles in immune evasion, as they inhibit phagocytosis, as well as protecting the bacteria while outside the host. Another group of virulence factors possessed by bacteria are immunoglobulin (Ig) proteases.
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Some bacteria, such as Streptococcus pyogenes, Staphylococcus aureus and Pseudomonas aeruginosa, produce a variety of enzymes which cause damage to host tissues. Enzymes include hyaluronidase, which breaks down the connective tissue component hyaluronic acid; a range of proteases and lipases; DNases, which break down DNA, and hemolysins which break down a variety of host cells, including red blood cells. Virulence Factors basically Include the Antigenic Structure and The Toxins produced by the organisms.
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Eventually, PT causes lymphocytosis, one of the systemic manifestations of whooping cough. PT, a decisive virulence determinant of B. pertussis, is able to cross the blood–brain barrier by increasing its permeability. As a result, PT can cause severe neurological complications; however, recently it has been found that the medicinal usage of Pertussis toxin can promote the development of regulatory T cells and prevent central nervous system autoimmune disease, such as multiple sclerosis.
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Overview of the main types of viral infection and the most notable species involvedMainly Chapter 33 (Disease summaries), pp. 367–92 in: Examples of common human diseases caused by viruses include the common cold, influenza, chickenpox, and cold sores. Many serious diseases such as rabies, Ebola virus disease, AIDS (HIV), avian influenza, and SARS are caused by viruses. The relative ability of viruses to cause disease is described in terms of virulence.
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Anthrax is a disease caused by Bacillus anthracis, a spore-forming, Gram positive, rod-shaped bacterium (Fig. 1). The lethality of the disease is caused by the bacterium's two principal virulence factors: (i) the polyglutamic acid capsule, which is anti-phagocytic, and (ii) the tripartite protein toxin, called anthrax toxin. Anthrax toxin is a mixture of three protein components: (i) protective antigen (PA), (ii) edema factor (EF), and (iii) lethal factor (LF).
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Fimbriae are believed to be involved in attachment to solid surfaces or to other cells, and are essential for the virulence of some bacterial pathogens. Pili (sing. pilus) are cellular appendages, slightly larger than fimbriae, that can transfer genetic material between bacterial cells in a process called conjugation where they are called conjugation pili or sex pili (see bacterial genetics, below). They can also generate movement where they are called type IV pili.
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The Ti plasmid is responsible for transmission of crown gall disease in plants infected with A. vitis. Tumorigenic A. vitis transfers its Ti plasmid to other bacteria, and transfers T-DNA into plants. Virulence genes encoded by the Ti plasmid generate single-strand T-DNA molecules, which in turn are transferred to healthy hosts. Disorganized cell division occurs in infected hosts, leading to gall development instead of the formation of healthy vascular tissue.
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Its receptor ectodomain recognizes the cleaved form of the cytokine Spätzle, which is secreted in the haemolymph as an inactive dimeric precursor. The Toll receptor shares the cytoplasmatic TIR domain with mammalian TLRs, but the ectodomain and intracytoplasmatic tail are different. This difference might reflect a function of these receptors as cytokine receptors rather than PRRs. The Toll pathway is activated by different stimuli, such as Gram positive bacteria, fungi and virulence factors.
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Pseudomonas syringae causes bacterial speck disease in tomatoes by hijacking the plant's jasmonate (JA) signaling pathway. This bacteria utilizes a type III secretion system to inject a cocktail of viral effector proteins into host cells. One of the molecules included in this mixture is the phytotoxin coronatine (COR). JA- insensitive plants are highly resistant to P. syringae and unresponsive to COR; additionally, applying MeJA was sufficient to rescue virulence in COR mutant bacteria.
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Bordetella pertussis is a Gram-negative, aerobic, pathogenic, encapsulated coccobacillus of the genus Bordetella, and the causative agent of pertussis or whooping cough. Like B. bronchiseptica, B. pertussis is motile and expresses a flagellum-like structure. Its virulence factors include pertussis toxin, adenylate cyclase toxin, filamentous hæmagglutinin, pertactin, fimbria, and tracheal cytotoxin. The bacterium is spread by airborne droplets; its incubation period is 7–10 days on average (range 6–20 days).
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A report released in 2013 by the Center for Disease Control (CDC) estimated that each year in the United States, at least 2 million people get an antibiotic-resistant bacterial infection, and at least 23,000 people die from those infections. Due to their indispensability in Bacteria, essential persistent DNA methyltransferases are potential targets for the development of epigenetic inhibitors capable of, for example, enhance the therapeutic activity of antimicrobials , or decrease a pathogen's virulence .
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Adhesion can be a critical determinant of virulence for bacteria. The ability to attach to host cells allows bacteria to interact with them in various ways, whether by type III secretion system or simply by holding on against the prevailing movement of fluids. Outer membrane protein A (OmpA) has been shown to be involved in the adherence of A. baumannii to epithelial cells. This allows the bacteria to invade the cells through the zipper mechanism.
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SprD is located between genes scn and chp in the innate immune evasion cluster (IEC) of the S. aureus genome. Its placement within this region was the first indication of a virulence-factor regulatory function. SprD binds with sbi (Staphylococcus aureus binder of IgG) mRNA which encodes an immune evasion protein. It occludes the Shine-Dalgarno sequence and the initiation codon of sbi, forming a sbi mRNA-SprD duplex repressing the translation of the mRNA.
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An estimated 100,000 people perished. Typhus appeared again in the late 1830s, and yet another major typhus epidemic occurred during the Great Irish Famine between 1846 and 1849. The Irish typhus spread to England, where it was sometimes called "Irish fever" and was noted for its virulence. It killed people of all social classes, as lice were endemic and inescapable, but it hit particularly hard in the lower or "unwashed" social strata.
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Plants have evolved efficient defense systems against pathogenic microbes. A rapid plant defense reaction after pathogen attack is the oxidative burst, which involves the production of reactive oxygen species at the site of the attempted invasion. As a pathogen, U. maydis can respond to such an oxidative burst by an oxidative stress response, regulated by gene YAP1. This response protects U. maydis from the host attack, and is necessary for the pathogen’s virulence.
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The normal flora of the upper airway give protection by competing with pathogens for nutrients. In the lower airways, reflexes of the glottis, actions of complement proteins and immunoglobulins are important for protection. Microaspiration of contaminated secretions can infect the lower airways and cause pneumonia. The progress of pneumonia is determined by the virulence of the organism; the amount of organism required to start an infection; and the body's immune response against the infection.
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In that role, he became a hated figure of the left, because of his determination to expropriate the land of 107 peasant farmers and shepherds on the Larzac plateau, to extend an existing military base. The resulting civil disobedience campaign was ultimately victorious. Considered as a guardian of the Gaullist orthodoxy, he was marginalized after the election of Valéry Giscard d'Estaing as President of France in 1974. He criticized with virulence his foreign policy.
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The PrfA thermoregulator UTR is an RNA thermometer found in the 5' UTR of the prfA gene. In Listeria monocytogenes, virulence genes are maximally expressed at 37 °C (human body temperature) but are almost silent at 30 °C. The genes are controlled by PrfA, a transcriptional activator whose expression is thermoregulated. It has been shown that the untranslated mRNA (UTR) preceding prfA, forms a secondary structure, which masks the ribosome binding region.
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Further this fragment can be incorporated into a host genome. Agrobacterium has been known to evolve a control system that hijacks host factors and cellular processes for several pathways of host-plant defense response to invade the host cell nucleus. For the integration of T-DNA into the target host genome, Agrobacterium carries out multiple interactions with host-plant factors. To interact with host plant proteins many Agrobacterium virulence proteins encoded by vir genes.
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Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and establishment of disease in the host. Sepsis caused by gram- negative bacteria is thought to be largely due to a response by the host to the lipid A component of lipopolysaccharide, also called endotoxin. Sepsis caused by gram-positive bacteria may result from an immunological response to cell wall lipoteichoic acid. Bacterial exotoxins that act as superantigens also may cause sepsis.
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Tsh-associated self-cleaving domain (Escherichia coli) and similar Autotransporter proteins are outer membrane or secreted proteins found in a broad variety of Gram-negative bacteria. These proteins contain three structural motifs: a signal sequence, a passenger domain located at the N-terminal, and a translocator or autotransporter domain located at the C-terminal, forming a beta barrel structure. These structures promote the protein self-transport. Autotransporter proteins are usually related to virulence functions.
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On April 29, 2013, scientists in Rensselaer Polytechnic Institute, funded by NASA, reported that, during spaceflight on the International Space Station, microbes seem to adapt to the space environment in ways "not observed on Earth" and in ways that "can lead to increases in growth and virulence". Under certain test conditions, microbes have been observed to thrive in the near- weightlessness of space and to survive in the vacuum of outer space.
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The poem includes character sketches of "Atticus" (Joseph Addison) and "Sporus" (John Hervey). Addison is presented as having great talent that is diminished by fear and jealousy; Hervey is sexually perverse, malicious, and both absurd and dangerous.Rogers, The Alexander Pope Encyclopedia, p. 111. Pope marks the virulence of the "Sporus" attack by having Arbuthnot exclaim "Who breaks a butterfly upon a wheel?" in reference to the form of torture called the breaking wheel.
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In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its cell-wall polysaccharide, a virulence factor displayed on its surface. Later, in 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T-antigen. Four of the 20 T-antigens have been revealed to be pili, which are used by bacteria to attach to host cells. As of 2016, a total of 120 M proteins are identified.
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Recent studies have discovered that anaerobiosis can significantly impact the major regulatory circuit of quorum sensing. This important link between quorum sensing and anaerobiosis has a significant impact on the production of virulence factors of this organism. It is hoped that the therapeutic enzymatic degradation of the signaling molecules will prevent the formation of such biofilms and possibly weaken established biofilms. Disrupting the signaling process in this way is called quorum sensing inhibition.
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Her thesis Om Klebsiella (1956) was one of the first scientific papers addressing the presence of bacterial cross- infection. Together with her husband, she investigated the virulence factors and related properties of coliforms. The work led to the establishment of a coli department which became the World Health Organization's International Escherichia Centre, leading to a national Salmonella Centre and an international Klebsiella Centre. In 1968, she was appointed overlæge (head of department).
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The P1 antigen is the primary virulence factor of mycoplasma. P1 is a membrane associated protein that allows adhesion to epithelial cells. The P1 receptor is also expressed on erythrocytes which can lead to autoantibody agglutination from mycobacteria infection. Several Mycoplasma species can cause disease, including M. pneumoniae, which is an important cause of atypical pneumonia (formerly known as "walking pneumonia"), and M. genitalium, which has been associated with pelvic inflammatory diseases.
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Viruses rely on hijacking the cellular machinery of the cells they infect to create their own viral proteins and allow them to continue infecting new cells. Their ability to manipulate eIFs like eIF4A1, therefore, considerably impacts their virulence. For instance, cytomegalovirus relies on eIF4A to drive its protein synthesis. The viral protein pUL69 stabilizes the formation of eIF4F, through binding to eIF4A, a process by which eIF4E is prevented from dissociating from the eIF4F complex.
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It is thought that Ail directly promotes invasion and loop 2 contains an active site, perhaps a receptor-binding domain. The phage protein Lom is expressed during lysogeny, and encode host-cell envelope proteins. Lom is found in the bacterial outer membrane, and is homologous to virulence proteins of two other enterobacterial genera. It has been suggested that lysogeny may generally have a role in bacterial survival in animal hosts, and perhaps in pathogenesis.
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Much is unknown about the pathogenecity and virulence of Yokose virus. The strain XYBX1332 isolated in China was found to cause cytopathic effects in mammalian cells. In the study of fruit bats infected with Yokose virus, they did not observe any clinical signs of disease. However, a study conducted on bat alveolar epithelial cells and kidney cells found that infection of Yokose virus led to viral replication and cell death shortly after.
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On returning to the UK, in 1955, Dane was appointed lecturer in microbiology at Queen’s University, Belfast, where he worked with Professor George Dick on the recently developed attenuate and killed poliovirus vaccines. Through their research they established that the early live polio vaccines developed by Hilary Koprowski were unsafe because they could return to virulence when excreted by people given the vaccine. Professor Dick’s team also initiated studies of combined diphtheria/pertussis/tetanus vaccines.
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Population genetics is not the only relevant factor in an epidemic. Virulence factors are also important in causing disease, and population genetic studies struggle to monitor these. This is because the genes involved are often highly recombining and mobile between strains in comparison with the population genetic framework. Thus, for example in Escherichia coli, identifying strains carrying toxin genes is more important than having a population genetics-based evaluation of prevalent strains.
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P fimbriae (also known as pyelonephritis-associated pili) or P pili or Pap are chaperon-usher type fimbrial appendages found on the surface of many Escherichia coli bacteria. The P fimbriae is considered to be one of the most important virulence factor in uropathogenic E. coli and plays an important role in upper urinary tract infections. P fimbriae mediate adherence to host cells, a key event in the pathogenesis of urinary tract infections.
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However, certain infections have been shown to delay the removal of dead bodies or alter where they are placed.Fan, Yanhua, Pereira, Roberto M., Kilic, Engin, CAsella, George, Keyhani, Nemat O., "Pyrokinin b-Neuropeptide Affects Necrophoretic Behavior in Fire Ants (S. invicta), and Expression of b-NP in a Mycoinsecticide Increases Its Virulence" PLoS ONE, Vol. 7 Issue 1, January 2012 Although placing corpses farther away reduces the risk of infection, it also requires more energy.
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Like Unit 731, its more notorious counterpart, Unit 1855 devised virulent strains of bacteria and conducted lethal experiments on prisoners of war. Strains of infectious diseases developed by Unit 1855 were used about 70 times during the war, killing over 100,000 civilians in northern China. In 1943, a strain of cholera released by the unit in southern Beijing to test its virulence killed 1,872 residents. Biological warfare was banned by the Geneva Protocol of 1925.
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The filamentous haemagglutinin adhesin (FHA) is a large, filamentous protein that serves as a dominant attachment factor for adherence to host ciliated epithelial cells of the respiratory tract, called respiratory epithelium. It is associated with biofilm formation and possesses at least four binding domains which can bind to different cell receptors on the epithelial cell surface. One notable bacterium that produces filamentous haemagglutinin adhesin is Bordetella pertussis, which uses this protein as a virulence factor.
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Lysenin is a pore-forming toxin (PFT) present in the coelomic fluid of the earthworm Eisenia fetida. Pore-forming toxins are a group of proteins that act as virulence factors of several pathogenic bacteria. Lysenin proteins are chiefly involved in the defense against eukaryotic and prokaryotic pathogens. Following the general mechanism of action of PFTs lysenin is segregated as a soluble monomer that binds specifically to a membrane receptor, sphingomyelin in the case of lysenin.
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Teams from The Sainsbury Laboratory (TSL) and the John Innes Centre in Norwich sequenced the genome of the fungus in December 2012. The sequence has been published on the website OpenAshDieBack and offers clues to how the fungus infects trees. The study has uncovered toxin genes and other genes that may be responsible for the virulence of the fungus. In the long term researchers aim to find the genes that confer resistance to the pathogen on some ash trees.
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In conventional farming it is controlled by fungicide treatment of seeds. In organic farming seeds can be cleaned by brushing before sowing, but it is also desirable that plants have genetic resistance. A CCP, including crosses of resistant cultivars, was grown with heavy common bunt infection for 5 years and it appeared to get more resistant, but the common bunt's virulence appeared to change at least as fast. The overall result was that infection levels went up.
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Vaccination against An. marginale is done using live strains of the cross-reactive An. centrale. Vaccines are available on a commercial basis to immunize cattle against Babesia bovis. This is made by serial infection of calves to attenuate the virulence of the strain of Babesia, followed by splenectomy to produce many of the piroplasm stage in blood, which is then bottled for use. The vaccine is delivered containing the live protozoa to induce immunity without acute disease.
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The extensive similarity between E. coli and S. flexneri is proposed to be due to horizontal transfer. All of the genes needed for S. flexneri to invade the epithelial lining of the colon are found on a virulence plasmid called pINV. The genome of pINV is highly conserved between subspecies of S. flexneri. S. flexneri also has two other small multicopy plasmids, but some strains of S. flexneri have more plasmids that are suspected to confer antibiotic resistance.
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PlcR is a global transcriptional regulator which controls most of the secreted virulence factors in B. cereus and B. thuringiensis. It is chromosomally encoded and is ubiquitous throughout the cell. In B. anthracis, however, the plcR gene contains a single base change at position 640, a nonsense mutation, which creates a dysfunctional protein. While 1% of the B. cereus group carries an inactivated plcR gene, none of them carries the specific mutation found only in B. anthracis.
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B. anthracis possesses an antiphagocytic capsule essential for full virulence. The organism also produces three plasmid-coded exotoxins: edema factor, a calmodulin-dependent adenylate cyclase that causes elevation of intracellular cAMP and is responsible for the severe edema usually seen in B. anthracis infections, lethal toxin which is responsible for causing tissue necrosis, and protective antigen, so named because of its use in producing protective anthrax vaccines, which mediates cell entry of edema factor and lethal toxin.
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Several draft genomes from whole genome sequencing have been published. C.auris has a genome size of 12.3–12.5 Mb with a GC-content of 44.5–44.8%. The C.auris genome was found to encode several genes for the ABC transporter family, a major facilitator superfamily, which helps to explain its multiple drug resistance. Its genome also encodes virulence-related gene families such as lipases, oligopeptide transporters, mannosyl transferases and transcription factors which facilitate colonization, invasion, and iron acquisition.
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300px If an allele provides a fitness benefit, its frequency will increase within a population – selection is directional or positive. Selective sweeps are one form of directional selection, where the increase in frequency will eventually lead to the fixation of the advantageous allele. The process is considered to be slower in comparison to negative frequency dependent selection. It may produce an "arms race", consisting of the repeated origin and fixation of new parasite virulence and host defence traits.
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These circular plasmids consist of a conserved backbone responsible for replication and bacterial conjugation of the plasmid. This portion of the plasmid is highly conserved and found in nonpathogenic Rhodococci plasmids. In addition to the conserved region, the virulence plasmids contain a highly variable region that has undergone substantial genetic rearrangements, including inversion and deletions. This region has a different GC-content from the rest of the plasmid, and is flanked by genes associated with mobile genetic elements.
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However, due in part to the small size of many PSMs, they have largely gone unnoticed until recent years. Although PSMs are present in every Staphylococcal species, there is still diversity. Staphylococcus aureus encodes eight different PSMs, PSMα 1-4, PSMβ 1-2, PSMγ (Also known as δ-toxin in S. aureus), and PSM-mec.Li S, Huang H, Rao X, Chen W, Wang Z, Hu X. Phenol-soluble modulins: novel virulence-associated peptides of staphylococci REVIEW.
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The signaling molecules used by multicellular organisms are often called pheromones. They can have such purposes as alerting against danger, indicating food supply, or assisting in reproduction. In unicellular organisms such as bacteria, signaling can be used to 'activate' peers from a dormant state, enhance virulence, defend against bacteriophages, etc. In quorum sensing, which is also found in social insects, the multiplicity of individual signals has the potentiality to create a positive feedback loop, generating coordinated response.
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It occurs worldwide in both epidemic and endemic form. N. meningitidis is spread through saliva and respiratory secretions during coughing, sneezing, kissing, chewing on toys and even through sharing a source of fresh water. It has also been reported to be transmitted through oral sex and cause urethritis in men. It infects its host cells by sticking to them with long thin extensions called pili and the surface-exposed proteins Opa and Opc and has several virulence factors.
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In molecular biology, the haemolysin expression modulating protein family is a family of proteins. This family consists of haemolysin expression modulating protein (Hha) from Escherichia coli and its enterobacterial homologues, such as YmoA from Yersinia enterocolitica, and RmoA encoded on the R100 plasmid. These proteins act as modulators of bacterial gene expression. Members of this family act in conjunction with members of the H-NS family, participating in the thermoregulation of different virulence factors and in plasmid transfer.
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CRISPR-Cas-based "RNA-guided nucleases" can be used to target virulence factors, genes encoding antibiotic resistance, and other medically relevant sequences of interest. This technology thus represents a novel form of antimicrobial therapy and a strategy by which to manipulate bacterial populations. Recent studies suggest a correlation between the interfering of the CRISPR-Cas locus and acquisition of antibiotic resistance. This system provides protection of bacteria against invading foreign DNA, such as transposons, bacteriophages, and plasmids.
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The lethality of the anthrax disease is due to the bacterium's two principal virulence factors: the poly-D-glutamic acid capsule, which protects the bacterium from phagocytosis by host neutrophils, and the tripartite protein toxin, called anthrax toxin. Anthrax toxin is a mixture of three protein components: protective antigen (PA), edema factor (EF), and lethal factor (LF). PA plus LF produces lethal toxin, and PA plus EF produces edema toxin. These toxins cause death and tissue swelling (edema), respectively.
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For instance, in the causative agent of plague (Yersinia pestis), the loss of the T3SS is sufficient to render the bacteria completely avirulent, even when they are directly introduced into the bloodstream. Gram negative microbes are also suspected to deploy bacterial outer membrane vesicles to translocate effector proteins and virulence factors via a membrane vesicle trafficking secretory pathway, in order to modify their environment or attack/invade target cells, for example, at the host-pathogen interface.
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Multiple mutations are needed for the virus to grow at cold temperatures, so this process is effectively irreversible and once the virus has lost virulence (become "attenuated"), it will not regain the ability to infect people. The attenuated virus is then grown in chicken eggs as before. The virus-containing fluid is harvested and the virus purified by filtration; this step also removes any contaminating bacteria. The filtered preparation is then diluted into a solution that stabilizes the virus.
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Analysis of CRISPR sequences revealed coevolution of host and viral genomes. Cas9 proteins are highly enriched in pathogenic and commensal bacteria. CRISPR/Cas-mediated gene regulation may contribute to the regulation of endogenous bacterial genes, particularly during interaction with eukaryotic hosts. For example, Francisella novicida uses a unique, small, CRISPR/Cas- associated RNA (scaRNA) to repress an endogenous transcript encoding a bacterial lipoprotein that is critical for F. novicida to dampen host response and promote virulence.
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RNA-Seq of human pathogens has become an established method for quantifying gene expression changes, identifying novel virulence factors, predicting antibiotic resistance, and unveiling host-pathogen immune interactions. A primary aim of this technology is to develop optimised infection control measures and targeted individualised treatment. Transcriptomic analysis has predominantly focused on either the host or the pathogen. Dual RNA-Seq has been applied to simultaneously profile RNA expression in both the pathogen and host throughout the infection process.
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Pseudomonas syringae produces polysaccharides which allow it to adhere to the surface of plant cells. It also releases quorum sensing molecules, which allows it to sense the presence of other bacterial cells nearby. If these molecules pass a threshold level, the bacteria change their pattern of gene expression to form a biofilm and begin expression of virulence-related genes. The bacteria secrete highly viscous compounds such as polysaccharides and DNA to create a protective environment in which to grow.
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In oysters the pathogen can cause deformities of the cilia as well as disfigurements of the velum, and eventually death. V. coralliilyticus also kills bacterial cells as well utilizing a Type VI secretion system to kill competitors, even out competing Vibrio cholerae cells in a bacterial killing assay. V. coralliilyticus possesses a host of virulence factors that contribute to its pathogenicity. It has been found to utilize several proteases, secretion systems, hemolysins, resistance factors, and quorum sensing.
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Aerobactin is a bacterial iron chelating agent (siderophore) found in E. coli. It is a virulence factor enabling E. coli to sequester iron in iron-poor environments such as the urinary tract. Aerobactin is biosynthesized by the oxidation of lysine, catalyzed by the enzyme aerobactin synthase, which is then coupled to citric acid. The gene for this enzyme is found in the aerobactin operon, which is roughly 8 kilobases long and contains 5 or more genes in total.
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LuxS is an important protein involved in quorum sensing, particularly in the synthesis of autoinducer molecules. Quorum-sensing E. coli regulator A (QseA) is found in LuxS systems and activates transcription of ler. Fis, a nucleoid associated protein essential for EPEC's ability to form attaching and effacing lesions, partly acts through activation of Ler expression. BipA, a ribosomal binding GTPase and prolific regulator of EPEC virulence, transcriptionally regulates Ler from an upstream position where it also regulates other genes.
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This inactivation is termed vertical inactivation, meaning that the DNA transposon is inactive and remains as a fossil. This type of transfer is not the most common, but has been seen in the case of the wheat virulence protein ToxA, which was transferred between the different fungal pathogens Parastagonospora nodorum, Pyrenophora tritici-repentis, and Bipolaris sorokiniana. Other examples include transfer between marine crustaceans, insects of different orders, and organisms of different phyla, such as humans and nematodes.
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The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence and 176 genes that maintain a noninvasive phenotype. Genetic information can vary up to 10% between strains. The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different lantibiotics.
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One of the virulence factors of C. difficile that largely constitutes its resistance to antibiotics is its toxins: enterotoxin TcdA and cytotoxin TcdB. Toxins produce spores that are difficult to inactivate and remove from the environment. This is especially true in hospitals where an infected patient's room may contain spores for up to 20 weeks. Combating the threat of the rapid spread of CDIs is therefore dependent on hospital sanitation practices removing spores from the environment.
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Phylogenetic studies performed on partial sequences of viruses from India suggest that additional genogroups exist. An analysis of strains isolated in Europe (Austria, France and Germany) showed that the clades C1b and C2b originated in 1994 (95% confidence interval 1992.7–1995.8) and 2002 (95% confidence interval 2001.6–2003.8), respectively. Intra- and inter-typic recombination occur commonly in EV-A71 virus infections.Huang SW, Cheng D, Wang JR. Enterovirus A71: virulence, antigenicity, and genetic evolution over the years.
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Virulent viruses such as HIV, which causes AIDS, have mechanisms for evading host defenses. HIV infects T-Helper Cells, which leads to a reduction of the adaptive immune response of the host and eventually leads to an immunocompromised state. Death results from opportunistic infections secondary to disruption of the immune system caused by AIDS. Some viral virulence factors confer ability to replicate during the defensive inflammation responses of the host such as during virus-induced fever.
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Gastric MALT lymphoma is frequently associated (72–98%) with chronic inflammation as a result of the presence of Helicobacter pylori, potentially involving chronic inflammation, or the action of H. pylori virulence factors such as CagA. The initial diagnosis is made by biopsy of suspicious lesions on esophagogastroduodenoscopy (EGD, upper endoscopy). Simultaneous tests for H. pylori are also done to detect the presence of this microbe. In other sites, chronic immune stimulation is also suspected in the pathogenesis (e.g.
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Death usually occurs within 5 days after onset of symptoms. The clinical signs of DEV "vary with virulence of virus strain, species, sex, and immune system status" of the host. Due to the formation of diphtheroid plaques on the eyelids and the mucosae of the respiratory system and gastrointestinal system the bird may show ophthalmic signs and refuse to drink. Blue winged teal can be infected by DEV, but are one of the most susceptible species.
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The epidemiology of Aujeszky's disease varies with the pathogenicity or virulence of the virus strain involved. This is best illustrated by the development of the severity of the disease in Denmark, where import of swine had been forbidden for decades up to 1972. Before 1964 only genital strains were spread, but then respiratory strains appeared, which subsequently were spread rapidly over the country, mainly by the trade of animals. In the late 1970s more virulent strains developed.
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CFP-10 also known as ESAT-6-like protein esxB or secreted antigenic protein MTSA-10 or 10 kDa culture filtrate antigen CFP-10 is a protein that is encoded by the esxB gene. CFP-10 is a 10 kDa secreted antigen from Mycobacterium tuberculosis. It forms a 1:1 heterodimeric complex with ESAT-6. Both genes are expressed from the RD1 region of the bacterial genome and play a key role in the virulence of the infection.
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Even if susceptible individuals remain, their contacts are likely to be immunized, preventing any further spread of the infection. The proportion of immune individuals in a population above which a disease may no longer persist is the herd immunity threshold. Its value varies with the virulence of the disease, the efficacy of the vaccine, and the contact parameter for the population. That is not to say that an outbreak can't occur, but it will be limited.
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Following internalization, the bacterium must escape from the vacuole/phagosome before fusion with a lysosome can occur. Three main virulence factors that allow the bacterium to escape are listeriolysin O (LLO- encoded by hly) phospholipase A (encoded by plcA) and phospholipase B (plcB). Secretion of LLO and PlcA disrupts the vacuolar membrane and allows the bacterium to escape into the cytoplasm, where it may proliferate. Once in the cytoplasm, L. monocytogenes exploits host actin for the second time.
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A recent model by Restif and Koella (2003) found that plant tolerance can directly impose photosynthetic on pathogens. Assuming that investment in tolerance will reduce plant fecundity, infection by pathogens will decrease the number of uninfected hosts. There may then be photosynthetic for decreased virulence in the pathogens, so that their plant host will survive long enough to produce enough offspring for future pathogens to infect (Restif and Koelle 2003). However, this may only have limited application to herbivores.
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Lactococcus garvieae in humans is a rare pathogen and of low virulence. More than 31 cases of infection in humans have been reported. These include 25 cases of endocarditis and other infections like those related to peritoneal dialysis catheters, discitis, catheter associated UTI, post TURP infection, liver abscess in a patient with cholangiocarcinoma, AICD/Pacemaker related infections to name a few. The signs and symptoms of United States cases ranges from urinary tract, blood, skin and pneumonic processes.
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George D. Heist (1886–1920) was an immunologist specializing in the study of infections of meningococcal bacteria that often result in meningococcal disease, which is well known as highly lethal and debilitating, and extremely difficult to treat. In 1919, Dr Heist and co-workers [Heist et al., 1922]Heist GD, Solis-Cohen S, Solis-Cohen M. (1922). A study of the virulence of meningococci for man and of human susceptibility to meningococcic infection. J Immunol;7:1–33.
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Sometimes, the protein domains targeted by the virulence factors are integrated into the NLRs. An example of this can be observed in plant resistance to the rice blast pathogen, where the RGA5 NLR has a heavy- metal-associated (HMA) domain integrated into its structure, which is targeted by multiple effector proteins. An example of indirect recognition: AvrPphB is a type III effector protein secreted by Pseudomonas syringae. This is a protease which cleaves a cellular kinase called PBS1.
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M protein is a virulence factor that can be produced by certain species of Streptococcus. Viruses, parasites and bacteria are covered in protein and sugar molecules that help them gain entry into a host by counteracting the host's defenses. One such molecule is the M protein produced by certain streptococcal bacteria. At its C-terminus within the cell wall, M proteins embody a motif that is now known to be shared by many Gram-positive bacterial surface proteins.
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Newton was criticized for the virulence of her anti-Zionist activity, which stretched to publishing in 1946 a defence of Mohammad Amin al-Husayni, the Grand Mufti of Jerusalem, who had met Adolf Hitler in 1941. The pamphlet, The Truth about the Mufti, was published by the Anglo-Arab Friendship Society, which she controlled, and excused his collaboration with the Nazis. In her autobiography, Fifty Years in Palestine, Newton blamed the British for the Mufti's relationship with Hitler.Karsh, Efraim.
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The cause of this disease is Yersinia pseudotuberculosis serotype O1. 95% are subtype O1b. Yersinia pseudotuberculosis has been divided into 6 genetic groups: group 1 has only been isolated from the Far East.Fukushima H Matsuda Y, Seki R, Tsubokura M, Takeda N, Shubin FN, Paik IK, Zheng XB (2001) Geographical heterogeneity between Far Eastern and Western countries in prevalence of the virulence plasmid, the superantigen Yersinia pseudotuberculosis-derived mitogen, and the high-pathogenicity island among Yersinia pseudotuberculosis strains.
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As early as 1976, low levels of maternal antibodies against the GBS capsular polysaccharide were shown to be correlated with susceptibility to GBS-EOD and GBS-LOD. Maternal-specific antibodies, transferred from the mother to the newborn, were able to confer protection to babies against GBS infection. The capsular polysaccharide of GBS, which is an important virulence factor, is also an excellent candidate for the development of an effective vaccine. GBS protein-based vaccines are also in development.
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His name is given to the old soccer stadium of Savannakhet, now a sports park. One day, after a game, Kou Voravong and friends gathered some coconuts from trees bordering the playground to satisfy their thirst. Madame Malpuech, the previous Commissioner's wife shouted at them, considering these behaviors as an act of vandalism on public property. As captain, he defended his teammates with such virulence that she filed complaint with the police against him for assaulting.
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In 2010, Sharma et al. presented a comprehensive analysis of transcription at single-nucleotide resolution by differential RNA-seq that confirmed the known acid induction of major virulence loci, such as the urease (ure) operon or the cag pathogenicity island (see below). More importantly, this study identified a total of 1,907 transcriptional start sites, 337 primary operons, and 126 additional suboperons, and 66 monocistrons. Until 2010, only about 55 transcriptional start sites (TSSs) were known in this species.
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The low GC-content of the cag PAI relative to the rest of the Helicobacter genome suggests the island was acquired by horizontal transfer from another bacterial species. The serine protease HtrA also plays a major role in the pathogenesis of H. pylori. The HtrA protein enables the bacterium to transmigrate across the host cells' epithelium, and is also needed for the translocation of CagA. The vacA gene codes for another major H. pylori virulence protein.
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It is common to speak of an entire species of bacteria as pathogenic when it is identified as the cause of a disease (cf. Koch's postulates). However, the modern view is that pathogenicity depends on the microbial ecosystem as a whole. A bacterium may participate in opportunistic infections in immunocompromised hosts, acquire virulence factors by plasmid infection, become transferred to a different site within the host, or respond to changes in the overall numbers of other bacteria present.
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Pathogenicity islands, relatively common genetic structures in bacterial pathogens, are composed of two or more adjacent genes that increase a pathogen's virulence. They may contain genes that encode toxins, coagulate blood, or as in this case, allow the bacteria to resist antibiotics. AbaR-type resistance islands are typical of drug-resistant A. baumannii, and different variations may be present in a given strain. Each consists of a transposon backbone of about 16.3 Kb that facilitates horizontal gene transfer.
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The cells' environmental conditions just after DNA replication determine whether Dam is blocked from methylating a region proximal to or distal from the promoter region. Once the pattern of methylation has been created, the pilus gene transcription is locked in the on or off position until the DNA is again replicated. In E. coli, these pili operons have important roles in virulence in urinary tract infections. It has been proposed that inhibitors of Dam may function as antibiotics.
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Although it was not recognized until the 1970s, nickel is known to play an important role in the biology of some plants, eubacteria, archaebacteria, and fungi. Nickel enzymes such as urease are considered virulence factors in some organisms. Urease catalyzes the hydrolysis of urea to form ammonia and carbamate. The NiFe hydrogenases can catalyze the oxidation of to form protons and electrons, and can also catalyze the reverse reaction, the reduction of protons to form hydrogen gas.
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In each plant species, Jander's laboratory uses techniques in biochemical genetics to identify the genetic causes of plant secondary metabolism involved in plant defenses against insects. Among his most cited work are studies of plant immunity to insects, map-based cloning in Arabidopsis, virulence of the bacteria Pseudomonas aeruginosa mutants in mice and insects, myrosinases and glucosinolates, green peach aphids (Myzus persicae), and epigenetic inheritance in plants. Jander has four children and is married to a geriatrician.
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The myxoma virus causes only a mild disease in these species, with symptoms limited to the formation of skin nodules. Myxomatosis is the name of the severe and often fatal disease in European rabbits caused by the myxoma virus. Different strains exist which vary in their virulence. The Californian strain, which is endemic to the west coast of the United States and Baja in Mexico, is the most virulent, with reported case fatality rates of 100%.
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At least five completely sequenced genomes of Coxiella burnetii exist, which contain about 2.1 Mbp of DNA each and encode around 2,100 open reading frames; 746 (or about 35%) of these genes have no known function. In bacteria small regulatory RNAs are activated during stress and virulence conditions. Coxiella burnetii small RNAs (CbSRs 1, 11, 12, and 14) are encoded within intergenic region (IGR). CbSRs 2, 3, 4 and 9 are located antisense to identified ORFs.
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En effet, > des le printemps 1919, des articles de presse commencent à associer > activisme et mouvement flamand; ce qui finira par créer l'image d'une > Flandre embochée.[...] À la fin de la guerre, les activistes wallons sont > jugés avec la même virulence que leurs homologues flamands et pour les mêmes > raisons. Mais, une fois condamnés, ils disparaissent des mémoires; alors que > l'activisme flamand est de plus en plus utilisé contre les revendications > flamandes.» Laurence Van Ypersele, ibid.
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The Journal of Medical Microbiology is a monthly peer-reviewed medical journal covering all aspects of microbiology relevant to human and animal disease, including pathogenicity, virulence, host response, epidemiology, microbial ecology, diagnostics, etc., relating to viruses, bacteria, fungi, and eukaryotic parasites. It is published by the Microbiology Society and the editors-in-chief are Norman Fry (Public Health England) and Kalai Mathee (Florida International University). The journal publishes primary research articles, reviews, short communications, personal views, and editorials.
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Another example is the association of infection with hepatitis B and hepatitis C viruses and liver cancer. Some subviral particles also cause disease: the transmissible spongiform encephalopathies, which include Kuru, Creutzfeldt–Jakob disease and bovine spongiform encephalopathy ("mad cow disease"), are caused by prions, hepatitis D is due to a satellite virus. The study of the manner in which viruses cause disease is viral pathogenesis. The degree to which a virus causes disease is its virulence.
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Their only proteolytic activity is releasing the virulence factor from the precursor, enabling it to be secreted. The active site residues in family N4 asparagine peptide lyases are N1100, Y1227, E1249 and R1282. Family N6 includes autoprocessing endopeptidases involved in type III protein secretion system, in which autoproteolysis is essential for mediating the secretion of proteins. Type III secretion system secretes proteins directly into host cells by an injectisome, a hollow tubular structure that penetrates into the host cell.
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Likewise, genetic resistance against the virus can develop in a host population over time. An example of the evolution of virulence in emerging virus is the case of myxomatosis in rabbits. The release of wild European rabbits in 1859 into Victoria, Australia for sport resulted in a rabbit plague. In order to curb with rabbit overpopulation, myxoma virus, a lethal species-specific poxvirus responsible for myxomatosis in rabbits, was deliberately released in South Australia in 1950.
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The PB1-F2 > protein probably contributes to viral pathogenicity and might have an > important role in determining the severity of pandemic influenza. Until > H5N1, all known avian influenza viruses had a Glu at position 627, while all > human influenza viruses had a lysine. Recently, some 75% of H5N1 human virus > isolates identified in Vietnam had a mutation consisting of Lysine at > residue 627 in the PB2 protein; a change believed associated with high > levels of virulence.
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In addition, they are naturally resistant to a number of antibiotics that disrupt cell-wall biosynthesis, such as penicillin. Due to their unique cell wall, they can survive long exposure to acids, alkalis, detergents, oxidative bursts, lysis by complement, and many antibiotics. Most mycobacteria are susceptible to the antibiotics clarithromycin and rifamycin, but antibiotic-resistant strains have emerged. As with other bacterial pathogens, M. tuberculosis produces a number of surface and secreted proteins that contribute to its virulence.
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RNA thermometers regulate gene expression in response to temperature allowing pathogens like Yersinia to switch on silent genes after entering the host organism. Usually, RNA thermometers are located in the 5'UTR, but an intergenic RNA thermometer was found in Yersinia pseudotuberculosis. The LcrF RNA thermometer together with the termo-labile YmoA protein activates synthesis of the most crucial virulence activator LcrF (VirF). The RNA thermosensor sequence is 100% identical in all human pathogenic Yersinia species.
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The basis for the affinity of R. mackenziei for brain tissue is unknown but has been hypothesized to involve the fungal melanin which acts as a virulence factor by allowing it to evade a human host's immune system and cross the blood-brain barrier. Melanin also protects the fungal cell wall from hydrolysis by scavenging the free radicals and hypochlorite produced by the immune system as well as helping to prevent antifungal drugs from entering the fungal pathogen.
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Numerous bacterial small non- coding RNAs have been identified to play regulatory functions. Some can regulate the virulence genes. 150 unannotated sRNAs were identified by sequencing of Y. pseudotuberculosis RNA libraries from bacteria grown at 26 °C and 37 °C, suggesting they may play a role in pathogenesis. By using single- molecule fluorescence in situ hybridisation smFISH technique it was shown that the number of YSR35 RNA increased 2.5 times upon temperature shift from 25 °C to 37 °C.
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One study showed that developing a vaccine using a 103 to 105 dose of killed spores from a low- virulence strain of Loma salmonae resulted in rainbow trout producing 85% less xenomas in their gills after experimental infection (compared to the control). This ultimately offers much improved protection to microsporidial gill disease which is common amongst rainbow trout. Therapeutic drugs have proved ineffective at treating this disease and harvesting whole-spores is a relatively easy technique.
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Raymond responded by increasing the virulence of her attack on Stone in the published version of the manuscript: > Masculine behavior is notably obtrusive. It is significant that > transsexually constructed lesbian feminists have inserted themselves into > positions of importance and/or performance in the feminist community. Sandy > Stone, the transsexual engineer with Olivia Records, an "all-women" > recording company, illustrates this well. Stone is not only crucial to the > Olivia enterprise but plays a very dominant role there.
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Opines are used by the bacteria as sources of nitrogen and energy. Infected cells form crown gall or root tumors. The Ti and Ri plasmids are thus endosymbionts of the bacteria, which are in turn endosymbionts (or parasites) of the infected plant. The Ti and Ri plasmids can also be transferred between bacteria using a system (the tra, or transfer, operon) that is different and independent of the system used for inter-kingdom transfer (the vir, or virulence, operon).
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Less commonly, glomerulonephritis can develop in chronic cases secondary to immune complex deposition. The great variability of clinical signs in individual cases of FCV is related to the relative virulence of different strains of the virus. VS-FCV can cause a rapid epidemic, with a mortality rate of up to 67%. Initial clinical signs include discharge from the eyes and nose, ulceration in the mouth, anorexia, and lethargy, and occur in the first one to five days.
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Steffen Mueller is a virologist and was Assistant Professor at Stony Brook University in New York. Mueller received his Ph.D. in molecular microbiology from Stony Brook University in 2002 in the laboratory of Eckard Wimmer. Mueller is a co-developer of the platform technology dubbed SAVE (Synthetic Attenuated Virus Engineering), a method to produce weakened synthetic viruses that are permanently prevented from regaining virulence. The method may hold the key to a new class of antiviral, so-called live, or attenuated vaccines.
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The relationship between virulence and transmission is complex and has important consequences for the long term evolution of a pathogen. Since it takes many generations for a microbe and a new host species to co-evolve, an emerging pathogen may hit its earliest victims especially hard. It is usually in the first wave of a new disease that death rates are highest. If a disease is rapidly fatal, the host may die before the microbe can be passed along to another host.
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Consistent with this belief, the organism has been isolated from the center of a stone removed from a patient with persistent P. penneri bacteriuria. These data substantiate the need for species-level identification of P. penneri in the clinical setting. Several virulence factors of P. penneri can make infections from this invasive pathogen more pronounced, persistent, and harder to eradicate. These include adherence due to the presence of fimbriae or afimbrial adhesins, invasiveness, swarming phenomenon, hemolytic activity, urea hydrolysis, proteolysis, and endotoxicity.
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The project makes all sequence data publicly available through GenBank, an international, NIH-funded, searchable online database. This research helps to provide international researchers with the information needed to develop new vaccines, therapies and diagnostics, as well as improve understanding of the overall molecular evolution of Influenza and other genetic factors that determine their virulence. Such knowledge could not only help mitigate the impact of annual influenza epidemics, but could also improve scientific knowledge of the emergence of pandemic influenza viruses.
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PVL is expressed in Staphylococcus aureus (shown x 50,000) Panton–Valentine leukocidin (PVL) is a cytotoxin--one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. It is present in the majority of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. PVL creates pores in the membranes of infected cells.
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Acyl-homoserine-lactone synthase () is an enzyme with systematic name acyl-(acyl-carrier protein):S-adenosyl-L-methionine acyltranserase (lactone- forming, methylthioadenosine-releasing). This enzyme catalyses the following chemical reaction : acyl-[acyl-carrier protein] + S-adenosyl-L-methionine \rightleftharpoons [acyl-carrier protein] + S-methyl-5'-thioadenosine + N-acyl-L-homoserine lactone Acyl-homoserine lactones (AHLs) are produced by a number of bacterial species and are used by them to regulate the expression of virulence genes in a process known as quorum-sensing.
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The structure of the C-terminal domain has been solved and shown to have a C-lectin type of structure. It is the C-terminal domain that mediates attachment to Tir. It is a 94 kDa outer membrane protein encoded by eaeA gene in the locus of enterocyte effacement (LEE), a 35-Kb pathogenicity island. Mutations in the eaeA gene result in loss of ability to cause A/E lesions, and is required for full virulence in infected volunteers and animal models.
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Thus, S. aureus must make a trade-off to increase their success as a species, exchanging reduced virulence for increased drug resistance. Another barrier to evolution is the Sau1 Type I restriction modification (RM) system. This system exists to protect the bacterium from foreign DNA by digesting it. Exchange of DNA between the same lineage is not blocked, since they have the same enzymes and the RM system does not recognize the new DNA as foreign, but transfer between lineages is blocked.
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Identified Virulence Factors of UPEC : Adherence, State Key Laboratory for Moleclular Virology and Genetic Engineering, Beijing. Retrieved July 2011 The Dr adhesins bind Dr blood group antigen (Dra) which is present on decay accelerating factor (DAF) on erythrocytes and other cell types. There, the Dr adhesins induce the development of long cellular extensions that wrap around the bacteria, accompanied by the activation of several signal transduction cascades, including activation of PI-3 kinase. UPEC can evade the body's innate immune defences (e.g.
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Poulin observes that the widespread prophylactic use of anthelmintic drugs in domestic sheep and cattle constitutes a worldwide uncontrolled experiment in the life-history evolution of their parasites. The outcomes depend on whether the drugs decrease the chance of a helminth larva reaching adulthood. If so, natural selection can be expected to favour the production of eggs at an earlier age. If on the other hand the drugs mainly affects adult parasitic worms, selection could cause delayed maturity and increased virulence.
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Following her masters, Scoffield pursued her graduate training at Auburn University in Auburn, Alabama. She trained under Laura Silo-Suh in the Department of Biological Sciences and she explored the mechanisms by which Pseudomonas aeruginosa growth mechanisms and virulence factor production. P. aeruginosa infections are one of the leading causes of chronic pulmonary infections in cystic fibrosis patients, often resulting in mortality. Her work helped to explore which environmental factors and adaptations lead to persistent and severe infection in CF patients.
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It is presumed that superoxide kills bacteria directly, as the virulence of many pathogens is dramatically attenuated when their superoxide dismutase (SOD) genes are deleted. However, superoxide can also spontaneously form hydrogen peroxide that undergoes further reactions to generate other reactive oxygen species (ROS) like hypochlorous acid (the reactive agent in bleach). It may also inactivate critical metabolic enzymes, initiate lipid peroxidation, damage iron-sulphur clusters, and liberate redox-active iron, which allows the generation of indiscriminate oxidants such as the hydroxyl radical.
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The outer membrane of B. burgdorferi is composed of various unique outer surface proteins (Osp) that have been characterized (OspA through OspF). The Osp proteins are lipoproteins anchored by N-terminally attached fatty acid molecules to the membrane. They are presumed to play a role in virulence, transmission, or survival in the tick. OspA, OspB, and OspD are expressed by B. burgdorferi residing in the gut of unfed ticks, suggesting they promote the persistence of the spirochete in ticks between blood meals.
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Overall, B. burgdorferi's genome oddly consists of one megabase chromosome and a variety of circular and linear plasmids ranging in size from 9 to 62 kilobases. The megabase chromosome, unlike many other eubacteria, has no relation to either the bacteria's virulence or to the host-parasite interaction. Some of the plasmids are necessary for the B. burgdorferi life cycle but not for propagation of the bacteria in culture. The genomic variations of B. burgdorferi contribute to varying degrees of infection and dissemination.
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Because of similarities between the innate immune system of insects and mammals, insects can replace mammals in some types of studies. Drosophila melanogaster and the Galleria mellonella waxworm have been particularly important for analysis of virulence traits of mammalian pathogens. Waxworms and other insects have also proven valuable for the identification of pharmaceutical compounds with favorable bioavailability. The decision to adopt such models generally involves accepting a lower degree of biological similarity with mammals for significant gains in experimental throughput.
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Iron is a necessary cofactor for many enzymes, and can act as a catalyst in the electron transport system. A. fumigatus has two mechanisms for the uptake of iron, reductive iron acquisition and siderophore-mediated. Reductive iron acquisition includes conversion of iron from the ferric (Fe+3) to the ferrous (Fe+2) state and subsequent uptake via FtrA, an iron permease. Targeted mutation of the ftrA gene did not induce a decrease in virulence in the murine model of A. fumigatus invasion.
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McLaughlin joined University of North Carolina at Chapel Hill as a postdoctoral researcher, funded by a Seeding Postdoctoral Innovators in Research and Education (SPIRE) fellowship. She characterised proteins responsible for the transfer of antibiotic resistance and virulence in bacterial cells, as well as teaching the biology program. She was appointed a professor of practice at Lehigh University, where she started the PA DNA Day, a now annual celebration of DNA and genetics. She was in Paris during the November 2015 Paris attacks.
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Streptococcus pneumoniaeis part of the normal upper respiratory tract flora. As with many natural flora, it can become pathogenic under the right conditions, typically when the immune system of the host is suppressed. Invasins, such as pneumolysin, an antiphagocytic capsule, various adhesins, and immunogenic cell wall components are all major virulence factors. After S. pneumoniae colonizes the air sacs of the lungs, the body responds by stimulating the inflammatory response, causing plasma, blood, and white blood cells to fill the alveoli.
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Genomic evolution occurs via gene gain, gene loss, and genome rearrangement, and these "events" are observed in multiple pathogen genomes, with some bacterial pathogens experiencing all three. Pathogenomics does not focus exclusively on understanding pathogen-host interactions, however. Insight of individual or cooperative pathogen behavior provides knowledge into the development or inheritance of pathogen virulence factors. Through a deeper understanding of the small sub-units that cause infection, it may be possible to develop novel therapeutics that are efficient and cost- effective.
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It has been speculated that this ability to manipulate host cells results from environmental selective pressure by amoebae, a hypothesis first proposed by Arturo Casadevall under the term "accidental virulence". In human infection, C. neoformans is spread by inhalation of aerosolized basidiospores, and can disseminate to the central nervous system, where it can cause meningoencephalitis. In the lungs, C. neoformans cells are phagocytosed by alveolar macrophages. Macrophages produce oxidative and nitrosative agents, creating a hostile environment, to kill invading pathogens.
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Examples of virulence factors for Staphylococcus aureus are hyaluronidase, protease, coagulase, lipases, deoxyribonucleases and enterotoxins. Examples for Streptococcus pyogenes are M protein, lipoteichoic acid, hyaluronic acid capsule, destructive enzymes (including streptokinase, streptodornase, and hyaluronidase), and exotoxins (including streptolysin). Examples for Listeria monocytogenes include internalin A, internalin B, lysteriolysin O, and actA, all of which are used to help colonize the host. Examples for Yersinia pestis are an altered form of lipopolysaccharide, type three secretion system, and YopE and YopJ pathogenicity.
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The specificity is acquired by a two- residues combination (12 and 13 mer) in every tandem repeat that composes the central region; a change in a residue will result in a change of specificity towards a promoter. Finally, AAD is known as the cause of final transcription modulation, essential for virulence or avirulence. It has been recorded that Xam works with the activation of SWEET sugar transporters, promoting the efflux of glucose and sucrose to the apoplasm for bacterial benefit.
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Neighbor- joining trees were estimated from Alignment1, and the within host tree is based on data from patient 2. Trees were re-rooted using Path-o-gen using known sample dates. There is some evidence from comparative phylogenetic analysis and epidemic simulations that HIV adapts at the level of the population to maximize transmission potential between hosts. This adaptation is towards intermediate virulence levels, which balances the productive lifetime of the host (time until AIDS) with the transmission probability per act.
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The transmission probability of HIV per sexual act is positively correlated with viral load, thereby providing evidence of the trade-off between transmissibility and virulence. It is therefore theoretically possible that HIV evolves to maximize its transmission potential. Epidemiological simulation and comparative phylogenetic studies have shown that adaptation of HIV towards optimum SPVL could be expected over 100–150 years. These results depend on empirical estimates for the transmissibility of HIV and the lifespan of hosts as a function of SPVL.
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Increasing dominance of C. glabrata in northern Europe, the United States, and Canada has been observed while C. parapsilosis has become more prominent in southern Europe, Asia, and South America. Regional species distribution guides treatment recommendations since the species exhibit different susceptibilities to azole and echinocandin classes of antifungals. The virulence of Candida species differs considerably, with C. parapsilosis and C. krusei being less virulent than C. albicans, C. tropicalis, and C. glabrata. This variation is reflected in mortality rates.
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The severity of the illness depends on the virulence of the infecting organism, the resistance of the invaded tissues, and the general health of the woman. Organisms commonly producing this infection are Streptococcus pyogenes; staphylococci (inhabitants of the skin and of pimples, carbuncles, and many other pustular eruptions); the anaerobic streptococci, which flourish in devitalized tissues such as may be present after long and injurious labour and unskilled instrumental delivery; Escherichia coli and Clostridium perfringens (inhabitants of the lower bowel); and Clostridium tetani.
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An old enemy re- emerges: downy mildew rears its ugly head on cucumber, impacting growers up and down the Eastern U.S. American Vegetable Grower, Feb. pp. 14-15. Considered a highly destructive foliar disease of cucurbits, successful breeding in the mid-twentieth century provided adequate control of downy mildew in cucumber without the use of fungicides. The resurgence in virulence has caused growers great concern and substantial economic losses, while downy mildew in other cucurbit crops continues to be a yearly hindrance.
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Substrate proteins attached to cell walls by sortases include enzymes, pilins, and adhesion-mediating large surface glycoproteins. These proteins often play important roles in virulence, infection, and colonization by pathogens. Surface proteins not only promote interaction between the invading pathogen and animal tissues, but also provide ingenious strategies for bacterial escape from the host's immune response. In the case of S. aureus protein A, immunoglobulins are captured on the microbial surface and camouflage bacteria during the invasion of host tissues.
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In molecular biology, the FasX small RNA (fibronectin/fibrinogen- binding/haemolytic-activity/streptokinase-regulator-X) is a non-coding small RNA (sRNA) produced by all group A Streptococcus. FasX has also been found in species of group D and group G Streptococcus. FasX regulates expression of secreted virulence factor streptokinase (SKA), encoded by the ska gene. FasX base pairs to the 5' end of the ska mRNA, increasing the stability of the mRNA, resulting in elevated levels of streptokinase expression.
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The chvE-gguAB gene in Agrobacterium tumefaciens encodes glucose and galactose importers that are also associated with virulence. Transporters are extremely vital in cell survival such that they function as protein systems that counteract any undesirable change occurring in the cell. For instance, a potential lethal increase in osmotic strength is counterbalanced by activation of osmosensing ABC transporters that mediate uptake of solutes. Other than functioning in transport, some bacterial ABC proteins are also involved in the regulation of several physiological processes.
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Kamoun in 2017 Kamoun is known for his contributions to our understanding of plant diseases and plant immunity. He used genomics and molecular biology methods to obtain insights into the biology and evolution of eukaryotic plant pathogens. He discovered virulence effector families from plant pathogens and showed how they can modulate plant immunity. He demonstrated how antagonistic coevolution with host plants has impacted the architecture of pathogen genomes, accelerated the evolution of effector genes, and drove the emergence of immune receptor networks.
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Live attenuated vaccines are administered via a viral transport media containing the relevant viral particles. The media may be given orally, injected via a hypodermic needle or by inhalation with the method often dependent upon the source phage's virulence factors. A vaccine works by encouraging the creation of memory B and T cells specific for an antigen associated with the pathogen in question. Accordingly, a vaccine is only effective for as long as the body maintains a population of these cells.
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Horizontal gene transfer (HGT) is the transfer of genetic elements between cells other than parental inheritance. HGT is responsible for much of the spread of antibiotic resistance among bacteria. Gene cassettes containing antibiotic resistance genes, or other virulence factors such as exotoxins, can be transferred from cell to cell via phage, transduction, taken up from the environment, transformation, or by bacterial conjugation. The ability to transfer gene cassettes between organisms has played a large role in the evolution of prokaryotes.
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Cholera toxin interrupting regulation of adenyl cyclase inside the cell causing efflux of water and sodium into the intestinal lumen. V. cholerae pathogenicity genes code for proteins directly or indirectly involved in the virulence of the bacteria. To adapt the host intestinal environment and to avoid being attacked by bile acids and antimicrobial peptides, V. cholera used its outer membrane vesicles (OMVs). Upon entry, the bacteria sheds its OMVs, containing all the membrane modifications that make it vulnerable for the host attack.
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NADH eliminates potentially toxic hydrogen peroxide under aerobic growth conditions and represents an enzymatic defense available against H2O2-mediated oxidative stress. Second, the enzyme presents an additional mechanism for regeneration of the NAD+ essential to the strictly fermentative metabolism of this organism. The enzyme may also protect against exogenous H2O2 and contribute to bacterial virulence. The actual function of NADH peroxidases and oxidases in plants is still unclear, but they could act in early signaling of oxidative stress through producing H2O2.
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By 1967 pneumococcal transformation had been shown to occur in vivo naturally, and it was further shown that treatment with streptomycin during dual infection by two pneumococcal strains could increase transformation—and virulence—while for the first time pneumococcal transformation was shown to occur in the respiratory tract. In 1969 it was shown in vivo that during drug treatment of a host, pneumococci could acquire genes from antibiotic-resistant streptococci, already in the host, and thereby the pneumococci could become resistant to erythromycin.
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In Pseudomonas aeruginosa, the PrrF RNAs are required for the production of the Pseudomonas quinolone signal (PQS), a quorum sensing molecule that activates the expression of several virulence genes. The phenomenon is mediated by PrrF repressing the expression of enzymes that degrade anthranilic acid, which is the precursor for PQS synthesis.Oglesby, A.G., Farrow, J.M., 3rd, Lee, J.H., Tomaras, A.P., Greenberg, E.P., Pesci, E.C., and Vasil, M.L. (2008). The influence of iron on Pseudomonas aeruginosa physiology: a regulatory link between iron and quorum sensing.
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The virulence factor in all known cases are biosynthesized by the pathogenic fungus. In this case of the symbiosis between R. microsporus and B. rhizoxinica, the hosted bacteria population produces the causative agent of rice seedling blight. Toxin formation by the bacteria has been demonstrated in analogy with Koch's postulates through the discovery that rhizoxin-producing strains of R. microsporus contained symbionts. Removal of the symbionts from the host degraded rhizoxin production and the symbionts were then grown in pure culture.
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Because there would be no evolutionary advantage to a pathogen keeping a protein that only serves to have it recognised by the plant, it is believed that the products of Avr genes play an important role in virulence in genetically susceptible hosts. Example: AvrPto is a small triple-helix protein that, like several other effectors, is targeted to the plasma membrane by N-myristoylation. AvrPto is an inhibitor of PRR kinase domains. PRRs signal plants to induce immunity when PAMPs are detected.
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The expression of 'ler' activates the remaining genes in the pathogenicity island inducing virulence. -At the same time, the system FusKR inhibits the Z0461 gene, a fucose transporter. Inactivation of LEE genes ( ↑ [fucose] ) Fucose increases the activation of the FusKR system, which inhibits the z0461 gene, which controls the metabolism of fucose. This is a mechanisms that is useful to avoid the competition for fucose with other strains of E. coli which are usually more efficient at using fucose as a carbon source.
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Experiments involving the mating types suggest that the (+) mating type has higher virulence and causes more cases of infection. However, both strains demonstrate a positive result for their ability to hydrolyze the urea molecule, indicating the presence of the urease enzyme. A conducted study showed that a majority of tested isolates (>50%) of M. fulvum tested positive for urea hydrolysis within 0–7 days, and almost all isolates tested positive within 10–12 days, suggesting rapid growth of the organism.
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Nematodes like C. elegans eat bacteria and surprisingly C. elegans is killed when it is provided S. enterica as a food source. This killing is accompanied by a persistent infection of S. enterica in the C. elegans intestine. Importantly, Dr. Aballay has shown that several well-studied S. enterica virulence factors required for causing disease in mammalian hosts are also required for C. elegans killing. This validates the use of C. elegans as a host to model Salmonella infection in mammals, including humans.
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Expression of innate immune components at epithelial barriers furthermore facilitates pathogen detection given that expression of virulence factors and hence exposure of PAMPs is required for the breaching of these barriers during invasion, whereas these factors might be downregulated when the pathogen interacts with professional immune cells at later stages of infection. Epithelial inflammasomes have mainly been studied in the intestinal mucosa, but there is also evidence for inflammasomes in other types of epithelial such as the urinary bladder epithelium.
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This fact, their interaction with host cells and the broad occurrence of autotransporter encoding genes, bring up the possibility to represent therapeutic targets for the design of vaccines against Gram-negative pathogens.Wells TJ, Tree JJ, Ulett GC, Schembri MA. Autotransporter proteins: novel targets at the bacterial cell surface. (2007) 274(2), 163-72 Two of the families in which the MEROPS database classifies asparagine peptide lyases are autotransporter proteins, families N4 and N6. Family N4 includes secreted virulence factors, or autotransporters, from enterobacteria.
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The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells. SARS-CoV-2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response. Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).
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Nanobodies for photothermal therapy. Nanobodies, which are able to bind tumor antigens like 271x271px Single-domain antibodies have been tested as a new therapeutic tool against multiple targets. In mice infected with influenza A virus subtype H5N1, nanobodies directed against hemaglutinin suppressed replication of the H5N1 virus in vivo and reduced morbidity and mortality. Nanobodies targeting the cell receptor binding domain of the virulence factors toxin A and toxin B of Clostridium difficile were shown to neutralize cytopathic effects in fibroblasts in vitro.
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It is not clear how it leads to disease, but it may suppress the defense mechanisms that thaxtomin activates. Another gene cluster in the 87.22 strain is very similar to a cluster found in the Gram negative plant pathogens Pseudomonas syringae and Pectobacterium atrosepticum. The cluster produces coronafacic acid, part of the plant toxin coronatine which mimics the plant hormone jasmonate, contributing to virulence. In 2007 the transcriptional regulator txtR was identified which is a member of the AraC/XylS protein family.
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YopO is a potent inducer of human macrophage apoptosis. It has also been suggested that a bacteriophage – Ypφ – may have been responsible for increasing the virulence of this organism. Depending on which form of the plague with which the individual becomes infected, the plague develops a different illness; however, the plague overall affects the host cell’s ability to communicate with the immune system, hindering the body to bring phagocytic cells to the area of infection. Y. pestis is a versatile killer.
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These knobs are easily identified as conspicuous bumps on the infected RBCs from the early trophozoite stage onward. The malarial parasite cannot induce its virulence on RBCs without knobs. As many as 10,000 knobs are distributed throughout the surface of a mature infected RBC, and each knob is 50-80 nm in diameter. The export of pfEMP1 from Maurer's cleft to RBC membrane is mediated by binding of another protein produced by the parasite called knob-associated histidine-rich protein (KAHRP).
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Marc Van Montagu and Jozef Schell at the University of Ghent (Belgium) discovered the gene transfer mechanism between Agrobacterium and plants, which resulted in the development of methods to alter Agrobacterium into an efficient delivery system for gene engineering in plants. A team of researchers led by Dr Mary-Dell Chilton were the first to demonstrate that the virulence genes could be removed without adversely affecting the ability of Agrobacterium to insert its own DNA into the plant genome (1983).
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The name autotransporter derives from an initial understanding that the protein was self-sufficient in transporting the passenger domain through the outermembrane. This view has since been challenged by Benz and Schmidt. Secretion of polypeptide chains through the outer membrane of Gram-negative bacteria can occur via a number of different pathways. The type V(a), or autotransporter, secretion pathway constitutes the largest number of secreted virulence factors of any one of the seven known types of secretion in Gram-negative bacteria.
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Colonies that underwent random transposition events were identified by BamHI digestion and Southern blotting using an internal IS1096 DNA probe. Colonies were screened for attenuated multiplication to identify colonies with mutations in candidate virulence genes. Mutations leading to an attenuated phenotype were mapped by amplification of adjacent regions to the IS1096 sequences and compared with the published M. tuberculosis genome. In this instance transposon mutagenesis identified 13 pathogenic loci in the M. tuberculosis genome which were not previously associated with disease.
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A. pleuropneumoniae was found to be the causative agent for up to 20% of all bacterial pneumonia cases in swine. The main disease associated with this bacterium is porcine pleuropneumonia, a highly contagious respiratory disease, affecting primarily young pigs (usually less than 6 months). All of the symptoms and signs of porcine pleuropneumonia can be attributed to its virulence factors. The symptoms include respiratory distress, bloodstained discharge (usually frothy) from the mouth, fever, anorexia, mild diarrhea, cyanosis, lethargy, and spontaneous abortion in sows.
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The exact species of scuticociliate responsible for a given outbreak is often not identified. As a result, differences in virulence and disease course among different scuticociliates are not well characterized. In one study, infection by Miamiensis avidus was reported to have a higher mortality rate than Pseudocohnilembus persalinus, Pseudocohnilembus hargisi and Uronema marinum. Infections by U. marinum show a less severe disease course, possibly restricted to the skin surface; it has been suggested that this ciliate may be only a secondary pathogen.
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This protein degrades the outer membrane protein A (OmpA) of E. coli as well as the virulence factors of such bacteria as Shigella, Salmonella and Yersinia. Mutations in this gene are associated with cyclic neutropenia (CyN) and severe congenital neutropenia (SCN). This gene is clustered with other serine protease gene family members, azurocidin 1 and proteinase 3 genes, at chromosome 19pter. All 3 genes are expressed coordinately and their protein products are packaged together into azurophil granules during neutrophil differentiation.
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CBM 588 does not establish permanently in the gut, in common with other orally administered probiotic bacteria. CBM 588 for clinical use is produced by submerged anaerobic fermentation followed by centrifugation, drying, blending and packaging. The MIYAIRI 588 strain of C. butyricum does not carry any genes encoding any toxins and virulence factors associated with Clostridium or other enteropathogens. Absence of neurotoxin production has been demonstrated by polymerase chain reaction (PCR) and Southern blot hybridisation for type E botulinum toxin gene.
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Horizontal gene transfer is common among bacteria, even among very distantly related ones. This process is thought to be a significant cause of increased drug resistance when one bacterial cell acquires resistance, and the resistance genes are transferred to other species. Transposition and horizontal gene transfer, along with strong natural selective forces have led to multi-drug resistant strains of S. aureus and many other pathogenic bacteria. Horizontal gene transfer also plays a role in the spread of virulence factors, such as exotoxins and exoenzymes, amongst bacteria.
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C. glabrata is of special relevance in nosocomial infections due to its innately high resistance to antifungal agents, specifically the azoles. Besides its innate tolerance to antifungal drugs, other potential virulence factors contribute to C. glabrata pathogenicity. One of them is the expression of a series of adhesins genes. These genes, which in C. glabrata are mostly encoded in the subtelomeric region of the chromosome, have their expression highly activated by environmental cues, so that the organism can adhere to biotic and abiotic surfaces in microbial mats.
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A major phenotype and potential virulence factor that C. glabrata possesses is low-level intrinsic resistance to the azole medications, which are the most commonly prescribed antifungal (antimycotic) medications. These medications, including fluconazole and ketoconazole, are "not effective in 15–20% of cases" against C. glabrata. It is still highly vulnerable to polyene medications such as amphotericin B and nystatin, along with variable vulnerability to flucytosine and caspofungin. However, intravenous amphotericin B is a medication of last resort, causing among other side effects, chronic kidney failure.
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Hutcheson (1997) found that the tertiary and quaternary structures of protein elicitors are dependent on elicitor activity. Even so, resistant gene products are commonly found in Leucine rich repeat domains which is the extracellular domain of FLS2, and hrp genes are directly related to disease incitement and hypersensitive response to resistant plants. In short, the more elicitors that are present within flagellin perception, the more plant defense response will occur regardless of virulence. It is just more common for avirulent pathogen to produce more elicitors.
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A new role for eVP24 was found when its expression was monitored in rodent species where changes in eVP24 seemed to be responsible for enhancing virulence, indicating that adaption of Ebola in animal models occurs through mutations in eVP24. Additionally, eVP24 inhibits interferon signaling by competitively binding to karyopherins which blocks phosphorylated STAT1 nuclear import. In 2014, it was found that this mechanism interferes with the cells response to viral infection, which suppressed the innate immune response, allowing the virus to proliferate in the body.
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Genetic engineering can improve virulence, usually by adding more virulent proteins, increasing infection rate or enhancing spore persistence. Many of the disease carrying vectors are susceptible to entomopathogenic fungi. An attractive target for biological control are mosquitos, vectors for a range of deadly diseases, including malaria, yellow fever and dengue fever. Mosquitos can evolve quickly so it becomes a balancing act of killing them before the Plasmodium they carry becomes the infectious disease, but not so fast that they become resistant to the fungi.
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It is one of the bacteria that might be implicated in destructive periodontal disease. Although it has been found more frequently in localized aggressive periodontitis, prevalence in any population is rather high. It has also been isolated from actinomycotic lesions (mixed infection with certain Actinomyces species, in particular A. israelii). It possesses certain virulence factors that enable it to invade tissues, such as the pore-forming toxin leukotoxin A. It has also been isolated from women with bacterial vaginosis and as an etiologic agent in endocarditis.
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Iglewski's research has centered on the pathogenesis of the Pseudomonas aeruginosa bacterium. She discovered that a type I quorum sensing system globally regulated virulence in a human pathogen. She has discovered exoenzymes and toxins including exo S, a type 3 secreted Pseudomonas toxin. She is well known for describing the molecular mechanism of action of Pseudomonas toxin A. Her work with Peter Greenberg demonstrated that gram- negative bacteria produce AHL signals that control processes such as biofilm formation in neighboring cells of the same species.
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These adhesins specifically bind D-galactose-D-galactose moieties on the P blood-group antigen of erythrocytes and uroepithelial cells. Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual's susceptibility or non-susceptibility, respectively, to E. coli urinary tract infections. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells. Another virulence factor commonly present in UPEC is the Dr family of adhesins, which are particularly associated with cystitis and pregnancy-associated pyelonephritis.
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Competition between parasites can be expected to favour faster reproducing and therefore more virulent parasites, by natural selection. Biologists long suspected cospeciation of flamingos and ducks with their parasitic lice, which were similar in the two families. Cospeciation did occur, but it led to flamingos and grebes, with a later host switch of flamingo lice to ducks. Among competing parasitic insect-killing bacteria of the genera Photorhabdus and Xenorhabdus, virulence depended on the relative potency of the antimicrobial toxins (bacteriocins) produced by the two strains involved.
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Adenylate cyclase toxin (ACT or CyaA), is a primary virulence factor in Bordetella pertussis. CyaA is a multifunctional RTX family toxin that targets myeloid phagocytes, impairing the innate immune response and promoting B. pertussis colonization. The cyaA operon encodes the five proteins CyaA (RTX toxin), CyaC (CyaA activation protein), and the three T1SS proteins: CyaB (an ABC transporter) CyaD (a membrane fusion protein), and CyaE (an outer membrane protein). The CyaA protein contains an adenylate cyclase domain (AC domain) and a hemolytic/cytolytic domain.
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Phenol-soluble modulins (PSMs) are a family of small protein, that carry out a variety of functions, including acting as toxins, assisting in biofilm formation, and colony spreading. PSMs are produced by Staphylococcus bacteria including Methicillin-resistant Staphylococcus aureus (MRSA), and Staphylococcus epidermidis. Many PSMs are encoded within the core genome and can play an important virulence factor. PSMs were first discovered in S. epidermidis by Seymour Klebanoff and via hot-phenol extraction and were described as a pro-inflammatory complex of three peptides.1\.
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ICL has found to be important in human, animal, and plant pathogenesis. For several agricultural crops including cereals, cucumbers, and melons, increased expression of the gene encoding ICL is important for fungal virulence. For instance, increased gene expression of icl1 has been seen in the fungus Leptosphaeria maculans upon infection of canola. Inactivation of the icl1 gene leads to reduced pathogenicity of the fungus, which is thought to be a result of the inability of the fungus to use carbon sources provided by the plant.
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The pathogenesis of BPF is not well established but it is thought that patients become pharyngeal or conjunctival carriers of H. aegyptius, which is followed by spreading to the bloodstream. This hypothesis is supported by the isolation of from both the conjunctiva and oropharynx of documented BPF cases with H. aegyptius bacteremia. Possible virulence factors of H. aegyptius include lipooligosaccharides (LOS), capsular polysaccharides, pilus proteins (mediates adhesion to mucosal membrane), immunoglobulin A1 (IgA1), membrane associated proteins, and extracellular proteins. In a study conducted by Barbosa et al.
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This has been attributed to living in unsanitary conditions and crowded areas, where the risk of coming into contact with other individuals carrying B. quintana and ectoparasites (body lice) is increased. Also noteworthy, the increasing migration worldwide may also play a role in spreading trench fever, from areas where it is endemic to susceptible populations in urban areas. Recent concern is the possibility of the emergence of new strains of B. quintana through horizontal gene transfer, which could result in the acquisition of other virulence factors.
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S. pyogenes has a cell wall composed of branched polymers which sometimes contain M protein, a virulence factor that is highly antigenic. The antibodies which the immune system generates against the M protein may cross-react with heart muscle cell protein myosin, heart muscle glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction. However, the only proven cross-reaction is with perivascular connective tissue. This inflammation occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils and macrophages.
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They can make up a significant portion of an organism's genome, particularly in eukaryotes. In prokaryotes, TE's can facilitate the horizontal transfer of antibiotic resistance or other genes associated with virulence. After replicating and propagating in a host, all transposon copies become inactivated and are lost unless the transposon passes to a genome by starting a new life cycle with horizontal transfer. It is important to note that DNA transposons do not randomly insert themselves into the genome, but rather show preference for specific sites.
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Simplified scheme of the life cycle of Amyloodinium ocellatum. (Dr P. Beraldo, University of Udine) The lifecycle of A. ocellatum is direct and divided in three phases. In general, it can be completed in five to seven days when temperature and salinity are between 23-27°C and 30-35 ppt respectively. However, the parasite can also express its virulence in extreme conditions. In particular, lethal outbreaks were documented at high temperatures (more than 35°C) in both salt water (46 ppt) and brackish (7 ppt) environments.
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One of the hallmark features of Trichomonas vaginalis is the adherence factors that allow cervicovaginal epithelium colonization in women. The adherence that this organism illustrates is specific to vaginal epithelial cells (VECs) being pH, time and temperature dependent. A variety of virulence factors mediate this process some of which are the microtubules, microfilaments, bacterial adhesins (4), and cysteine proteinases. The adhesins are four trichomonad enzymes called AP65, AP51, AP33, and AP23 that mediate the interaction of the parasite to the receptor molecules on VECs.
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The disease has spread throughout the world, but its occurrence is sporadic and rare. There are several named strains of ectromelia virus that vary in virulence, including NIH-79, Wash-U, Moscow, Hampstead, St. Louis-69, Bejing-70, and Ishibashi I–III. The mousepox model presents an opportunity to study the components of the immune system that are required for an efficient immunological response to a natural poxvirus infection in a well-understood animal model that can be further manipulated by targeted inactivation or expression of genes.
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The cells of these species are covered in a thin layer of glycoprotein capsular material that has a gelatin-like consistency, and that among other functions, serves to help extract nutrients from the soil. The C. neoformans capsule consists of several polysaccharides, of which the major one is the immunomodulatory polysaccharide called glucuronoxylomannan (GXM). GXM is made up of the monosaccharides glucuronic acid, xylose and mannose and can also contain O-acetyl groups. The capsule is functioning as the major virulence factor in cryptococcal infection and disease.
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Patterns of viral genetic variation are therefore heavily influenced by how quickly transmission occurs and by which entities transmit to one another. Patterns of viral genetic variation will also be affected by selection acting on viral phenotypes. Although viruses can differ with respect to many phenotypes, phylodynamic studies have to date tended to focus on a limited number of viral phenotypes. These include virulence phenotypes, phenotypes associated with viral transmissibility, cell or tissue tropism phenotypes, and antigenic phenotypes that can facilitate escape from host immunity.
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Birds and ants are the most common predators of P. plantaginis, to which the moth has both general and specialized defense mechanisms. The blue tit (Cyanistes caeruleus) is a well known predator. Selection by predation can impact host immune defense, as demonstrated by an experiment measuring the virulence of a pathogen Serrate marcescens in Parasemia plantaginis larvae. Larvae with smaller warning signals had higher survival rates than those with larger warning signals, suggesting that developing a warning signal comes at the expense of immune function.
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RnaG is a small regulatory non-coding RNA encoded by the virulence plasmid of Shigella flexneri, a Gram-negative pathogenic bacterium that causes human bacillary dysentery. It is a first regulatory RNA characterised in S. flexneri. The RNA is 450 nucleotides long (which makes it one of the largest regulatory sRNAs) and it contains a region with specific secondary structure that interacts with icsA (virG) mRNA and forms a transcription terminator. Acting as antisense, RnaG is transcribed from the complementary strand of its target, icsA mRNA.
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Furthermore, expression of virulence factors will only take place when a sufficiently large population of bacteria is present, which is determined through quorum sensing. When successful, the common symptoms of bacterial blight will be seen, with the main effect on the plant being a reduction in photosynthetic leaf area. Generally, the amount of photosynthetic area lost is not enough to impede plant growth. As the plant continues to grow it overcomes the loss of photosynthetic area and reduction in yield, if there is any, is negligible.
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Additionally, certain strains of T. gondii can secrete a protein known as GRA15, activating the NF-κB pathway, which upregulates the pro-inflammatory cytokine IL-12 in the early immune response, possibly leading to the parasite's latent phase. The parasite's ability to secrete these proteins depends on its genotype and affects its virulence. The parasite also influences an anti-apoptotic mechanism, allowing the infected host cells to persist and replicate. One method of apoptosis resistance is by disrupting pro-apoptosis effector proteins, such as BAX and BAK.
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Commonly studied regulons in bacteria are those involved in response to stress such as heat shock. The heat shock response in E. coli is regulated by the sigma factor σ32 (RpoH), whose regulon has been characterized as containing at least 89 open reading frames. Regulons involving virulence factors in pathogenic bacteria are of particular research interest; an often-studied example is the phosphate regulon in E. coli, which couples phosphate homeostasis to pathogenicity through a two-component system. Regulons can sometimes be pathogenicity islands.
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Serratia secrete a host of virulence factors including prodigiosin, biosurfactants, DNAse, lipase, protease, gelatinase, hemolysin, chitinase, chloroperoxidase, and alkaline phosphatase. Prodigiosin, a growth pigment, is often used as a phenotypic identification marker of Serratia species due to its red colorization. Biosurfactants have been isolated from Serratia marcescens, Serratia rubidaea and Serratia surfactantfaciens for their range of applications including emulsification, surface, antifouling, antitumor, and antimicrobial activity. Endonucleases, such as DNAse, may aid in scavenging activity, allowing them to exploit the environment and maximize availability of nutrients.
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The virB operon is the largest operon in the vir region, encoding for 11 VirB proteins involved in the transfer process of T-DNA and bacterial proteins into host plant cells (see transfer apparatus below). The virC operon encodes for two proteins: VirC1 and VirC2. These proteins influence the pathogenesis of the Agrobacterium towards different plant hosts, and mutations can reduce but not remove the virulence of the bacteria. Both the virC and virD operons can be repressed by a chromosomally encoded protein known as Ros.
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VirD2, a relaxase, will then nick one of the DNA strands and remain bound to the DNA as it is transferred to the recipient cell. Within the recipient cell, VirD2 will also work together with VirE2 to direct the transferred DNA to the recipient cell's nucleus. There are suggestions that VirD2 may be phosphorylated and dephosphorylated by different proteins, affecting its ability to deliver DNA. Conversely, little is known about VirD3, and mutational analyses have not provided any support for its role in the virulence of Agrobacterium.
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Since the 1980s and early 1990s, the roles of TcdA and TcdB in C. difficile infection have been much debated. Previous reports with purified toxins indicated that TcdA alone was enough to cause symptoms of infection and TcdB was unable to do so unless combined with TcdA. A more recent experiment indicated that TcdB was, in fact, essential for virulence. Earlier research established TcdA strictly as an enterotoxin, and TcdB as a cytotoxin, but later both toxins were found to have the same mechanism of action.
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One major focus of his research at Kentucky was on mycoviruses that infect fungal pathogens of plants. He discovered and characterized a virus in the Totiviridae family that infects the fungal pathogen Helminthosporium victoriae, which causes the economically important disease Victoria blight in oats. Most fungal viruses do not affect their host but Ghabrial showed that the virus attenuates the virulence of the fungus. This raises the possibility that such viruses might in future be used in the biological control of plant diseases caused by fungi.
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For example, one such virulence factor is cord factor (trehalose dimycolate), which serves to increase survival within its host. Resistant strains of M. tuberculosis have developed resistance to more than one TB drug, due to mutations in their genes. In addition, pre-existing first-line TB drugs such as rifampicin and streptomycin have decreased efficiency in clearing intracellular M. tuberculosis due not being able to effectively penetrate the macrophage nicheSchaaf, K. et al. A Macrophage Infection Model to Predict Drug Efficacy Against Mycobacterium Tuberculosis.
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As an intracellular pathogen, M. tuberculosis is exposed to a variety of DNA-damaging assaults, primarily from host-generated antimicrobial toxic radicals. Exposure to reactive oxygen species and/or reactive nitrogen species causes different types of DNA damage including oxidation, depurination, methylation, and deamination that can give rise to single- and double-strand breaks (DSBs). DnaE2 polymerase is upregulated in M. tuberculosis by several DNA-damaging agents, as well as during infection of mice. Loss of this DNA polymerase reduces the virulence of M. tuberculosis in mice.
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Hypovirus CHV1 is the only hypovirus found in Europe up to 2000. It is known for reducing the virulence of the fungus that causes chestnut blight (i.e. hypovirulence). Cryphonectria parasitica, the ascomycete fungus, originated in Asia and causes the disease chestnut blight in several chestnut species (Castanea sp.). Although symptoms are mild in Asian chestnut species that have co-evolved with the fungus, they are very severe in the North American chestnut species C. dentata and also in the European sweet chestnut, C. sativa.
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The genus Exserohilum comprises dematiaceous fungi commonly associated with foliar plant diseases and rarely with human and animal phaeohyphomycosis. Fungi of this genus are characterized by the presence of melanin in their cell walls, which is thought to contribute to their virulence. Many Exserohilum species are plant pathogens that affect a wide range of plant species, especially grasses Poaceae, causing distinct leaf spots and blights. However, S. rostrata has also been shown to survive in human as well as animal hosts, indicating pathogenic versatility.
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P.aeruginosa strains which are unable to synthesise pyocyanin can still benefit from its effects if the strain has co-infected the lung with wild-type strains which can produce pyocyanin. Biosynthesis can be impaired by disrupting the aro pathway which is responsible for the synthesis of chorismic acid from shikimate. Chorismic acid is the precursor of pyocyanin. :shikimic acid → chorismic acid → phenazine-1-carboxylic acid → 5-methylphenazine-1-carboxylic acid betaine → pyocyanin The complete virulence of P. aeruginosa can only be experienced when pyocyanin is produced.
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The motif includes a conserved pentapeptide LPXTG, which precedes a hydrophobic C-terminal membrane spanning domain, which itself precedes a cluster of basic residues at the C-terminus. M protein is strongly anti-phagocytic and is the major virulence factor for group A streptococci (Streptococcus pyogenes). It binds to serum factor H, destroying C3-convertase and preventing opsonization by C3b. However plasma B cells can generate antibodies against M protein which will help in opsonization and further the destruction of the microorganism by the macrophages and neutrophils.
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The use of toxins to damage the host is a method deployed by many bacterial pathogens. The major virulence factor of C. perfringens is the CPE enterotoxin, which is secreted upon invasion of the host gut, and contributes to food poisoning and other gastrointestinal illnesses. It has a molecular weight of 35.3kDa, and is responsible for the disintegration of tight junctions between epithelial cells in the gut. This mechanism is mediated by host claudin-3 and claudin-4 receptors, situated at the tight junctions.
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Avian Flu vaccine development by Reverse genetics techniques from the National Institute of Allergy and Infectious Diseases A technique called reverse genetics allows scientists to manipulate the genomes of influenza viruses and to transfer genes between viral strains. The technique allows the rapid generation of seed viruses for vaccine candidates that exactly match the anticipated epidemic strain. By removing or modifying certain virulence genes, reverse genetics also can be used to convert highly pathogenic influenza viruses into vaccine candidates that are safer for vaccine manufacturers to handle.
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In organisms other than D. melanogaster, the promoter of the human and mouse IRF1 gene has been found to contain a DPE consensus sequence at the appropriate distance from the transcription start site. This promoter, too, does not contain a TATA box. DPE has also been reported to play role in primitive Eukaryote Entamoeba histolytica.Naiyer S, Kaur D, Ahamad J, Singh SS, Singh YP, Thakur V, Bhattacharya A, Bhattacharya S. Transcriptomic analysis reveals novel downstream regulatory motifs and highly transcribed virulence factor genes of Entamoeba histolytica.
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Group B streptococcal infection, also known as Group B streptococcal disease or just Group B strep, is the infection caused by the bacterium Streptococcus agalactiae (S. agalactiae) (also known as group B streptococcus or GBS). GBS infection can cause serious illness and sometimes death, especially in newborns, the elderly, and people with compromised immune systems. As other virulent bacteria, GBS harbours an important number of virulence factors, the most important are the capsular polysaccharide (rich in sialic acid), and a pore-forming toxin, β-haemolysin.
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An inactivated vaccine (or killed vaccine) is a vaccine consisting of virus particles, bacteria, or other pathogens that have been grown in culture and then lose disease producing capacity. In contrast, live vaccines use pathogens that are still alive (but are almost always attenuated, that is, weakened). Pathogens for inactivated vaccines are grown under controlled conditions and are killed as a means to reduce infectivity (virulence) and thus prevent infection from the vaccine. The virus is killed using a method such as heat or formaldehyde.
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Antibodies (anti-tetanus immunoglobulin) have been used in the treatment and prevention of tetanus since the 1910s, and this approach continues to be a useful way of controlling bacterial disease. The monoclonal antibody bezlotoxumab, for example, has been approved by the US FDA and EMA for recurrent Clostridium difficile infection, and other monoclonal antibodies are in development (eg. AR-301 for the adjunctive treatment of S. aureus ventilator-associated pneumonia). Antibody treatments act by binding to and neutralizing bacterial exotoxins and other virulence factors.
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Batai virus is geographically spread throughout Asia and Europe. It has been shown that batai viruses from Japan, Malaysia and India share homologies in the genomic sequence more so than when virus strains from Europe and Asia are compared to each other. Reassortment of the genome can have some serious effects. It has been observed that reassortment between the M segment and the S and L segments with another strain of Batai virus (BUNV) can cause an increase in the virulence of Batai virus.
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The Doctor and his companions decide to attract attention by starting a fire, succeeding in manoeuvring an aerosol can into the flames of the Bunsen burner gas outlet. This coincides with Smithers discovering the true virulence of DN6 and demanding Forester cease his licence application. In the lab, the makeshift bomb explodes in Forester’s face as PC Rowse arrives. Back in the TARDIS, the Doctor succeeds in returning the craft and crew to normal size, a process which cures Barbara of her infection by DN6.
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He built off of the discovery of Robert Koch, who found that if the bile from a rinderpest gall bladder were diluted with an equal amount of pure glycerin, it would lose its virulence and would be safe to inject after 10 days. This would provide immunity lasting several months. Bliss then deducted that if a cow was injected with a small quantity of rinderpest blood ten days after being injected with the bile, it would have immunity. He tested this and found he was correct.
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The genome of Flavobacterium psychrophilum consists of a circular chromosome of 2,861,988 bp, which is predicted to contain 2,432 protein-coding genes. Compared to environmental members of the family, it has a small genome probably related to its restricted ecological niche. The genome encodes 13 assumed secreted proteases that are involved in virulence and destruction of the host's tissues. Also, the genome encodes for bacterial hemolysins that cooperate with proteases for tissue destruction and thiol-activated cytolysins like proteins that are responsible for host tissue damage.
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Lesions of paracoccidioidomycosis on a Brazilian child Little is known about the epidemiology of the new species, as most previous epidemiological reports have focused on P. brasiliensis. Infection with the Paracoccidioides species, known as paracoccidioidomycosis, may be asymptomatic and subclinical, or may form into either acute/subacute (juvenile) or chronic (adult) forms of the disease. P. lutzii has less adhesion to lung cells than P. brasilensis, potentially explaining its decreased virulence. It is predominantly distributed in the Central west and Amazon regions of Brazil and Ecuador.
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Evolutionary history of the Myxoma virus in Europe and Australia Given the importance of viral evolution to disease emergence, pathogenesis, drug resistance, and vaccine efficacy, it has been well studied by theoreticians and experimentalists. The introductions of myxoma virus into European rabbit populations in Australia and France created natural experiments in virulence evolution. While initial viral strains were highly virulent, attenuated strains were soon recovered from the field. These attenuated strains, which allowed rabbits to survive longer, came to dominate because they were more readily transmitted.
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GAS infections can cause over 500,000 deaths per year. Despite the emergence of antibiotics as a treatment for group A β-hemolytic streptococcus, infection of GAS is an increasing problem, particularly on the continent of Africa. There are many other types of streptococci (species of Streptococcus), including group B streptococcus (Streptococcus agalactiae) and Streptococcus pneumoniae, which cause other types of infections and should not be confused with group A strep. Several virulence factors contribute to the pathogenesis of GAS, such as M protein, hemolysins, and extracellular enzymes.
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He has been working there ever since, lastly as a professor and Executive Academic Director. The focus of his scientific activities was on the characterization of the development of localized fungal infections of the skin and related mucosal surfaces. He concentrated on secreted aspartic proteases of Candida albicans as virulence factors and toll- like receptors as relevant mediators of the inflammatory host response. It was his prime concern to develop active pharmaceutical ingredients for the treatment and prevention of fungal infections reflecting the increased understanding of pathogenesis.
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Black colours appear on the plant because of the infection of its cellular system necessary for the multiplication of the oomycete infectious population. The parasite contains virulent-avirulent allelic combinations in several microsatellite loci, likewise the host contains several multiloci resistance genes (or R gene). That interaction is called gene-for-gene relationship and is, in general, widespread in plant diseases. Expression of genetic patterns in the two species is a combination of resistance and virulence characteristics in order to have the best survival rate.
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Bovine alphaherpesvirus 1 (BoHV-1) is a virus of the family Herpesviridae and the subfamily Alphaherpesvirinae, known to cause several diseases worldwide in cattle, including rhinotracheitis, vaginitis, balanoposthitis, abortion, conjunctivitis, and enteritis. BoHV-1 is also a contributing factor in shipping fever, also known as bovine respiratory disease (BRD). It is spread horizontally through sexual contact, artificial insemination, and aerosol transmission and it may also be transmitted vertically across the placenta. BoHV-1 can cause both clinical and subclinical infections, depending on the virulence of the strain.
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Salmonella encodes a LuxR homolog, SdiA, but does not encode an AHL synthase. SdiA detects AHLs produced by other species of bacteria including Aeromonas hydrophila, Hafnia alvei, and Yersinia enterocolitica. When AHL is detected, SdiA regulates the rck operon on the Salmonella virulence plasmid (pefI-srgD-srgA-srgB-rck-srgC) and a single gene horizontal acquisition in the chromosome srgE. Salmonella does not detect AHL when passing through the gastrointestinal tracts of several animal species, suggesting that the normal microbiota does not produce AHLs.
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Avian influenza viruses that cause HPAI are highly virulent, and mortality rates in infected flocks often approach 100%. LPAI viruses are generally of lower virulence, but these viruses can serve as progenitors to HPAI viruses. The current strain of H5N1 responsible for die-offs of domestic birds in Asia is an HPAI strain; other strains of H5N1 occurring elsewhere in the world are less virulent and, therefore, are classified as LPAI strains. All HPAI strains identified to date have involved H5 and H7 subtypes.
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The temperate phage escaping repression would be a disadvantage for the bacteria. On the other hand, the prophage may transfer genes that enhance host virulence and resistance to the immune system. Also, the repressor produced by the prophage that prevents prophage genes from being expressed confers an immunity for the host bacteria from lytic infection by related viruses. Another system, arbitrium, has recently been described for bacteriophages infecting several Bacillus species, in which the decision between lysis and lysogeny is transmitted between bacteria by a peptide factor.
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In terms of enzymology, a histidine kinase (, EnvZ, histidine protein kinase, protein histidine kinase, protein kinase (histidine), HK1, HP165, Sln1p) is an enzyme that catalyzes the chemical reaction :ATP + protein L-histidine \rightleftharpoons ADP + protein N-phospho-L-histidine. Thus, the two substrates of this enzyme are ATP and protein L-histidine, whereas its two products are ADP and protein N-phospho-L-histidine. This type of enzyme is involved in signal transduction pathways upstream of many cellular processes including various metabolic, virulence, and homeostatic pathways.
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Ysr141 sRNA was shown to regulate the synthesis of the type III secretion system (T3SS) effector protein YopJ. The Yop-Ysc T3SS is a critical component of virulence for Yersinia species. Many novel sRNAs were identified from Y. pestis grown in vitro and in the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them sR035 predicted to pair with SD region and transcription initiation site of a thermo-sensitive regulator ymoA, and sR084 predicted to pair with fur, ferric uptake regulator.
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A.66.2) The Polysaccharide Transport (PST) Family # One (OLF) specific for lipid-linked oligosaccharide precursors of glycoproteins in eukaryotes - (TC# 2.A.66.3) The Oligosaccharidyl-lipid Flippase (OLF) Family # One (MVF) lipid-peptidoglycan precursor flippase involved in cell wall biosynthesis - (TC# 2.A.66.4) The Mouse Virulence Factor (MVF) Family # One (AgnG) which includes a single functionally characterized member that extrudes the antibiotic, Agrocin 84 - (TC# 2.A.66.5) The Agrocin 84 Antibiotic Exporter (AgnG) Family # And finally, one (Ank) that shuttles inorganic pyrophosphate (PPi) - (TC# 2.
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There are numerous NPVs, many of which were isolated from the cabbage looper or the alfalfa looper. NPVs vary in infectivity and virulence. For example, the AcMNPV isolates are more infectious than the TnSNPV isolates in the first instar, while the TnSNPV isolates produced more occlusion bodies, protein structures that protect the virus and increase long term infectivity. TnSNPVs are their most lethal during the third and fourth instars; they have detrimental effects such as delayed development, reduced egg production, and fewer hatched eggs.
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It is hard to establish with certainty which diseases jumped from other animals to humans, but there is increasing evidence from DNA and RNA sequencing, that measles, smallpox, influenza, HIV, and diphtheria came to humans this way. Various forms of the common cold and tuberculosis also are adaptations of strains originating in other species. Some experts have suggested that all human viral infections were originally zoonotic. Zoonoses are of interest because they are often previously unrecognized diseases or have increased virulence in populations lacking immunity.
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Infectious bacteria of the species Vibrio shiloi are the bleaching agent of Oculina patagonica in the Mediterranean Sea, causing this effect by attacking the zooxanthellae. V. shiloi is infectious only during warm periods. Elevated temperature increases the virulence of V. shiloi, which then become able to adhere to a beta-galactoside-containing receptor in the surface mucus of the host coral. V. shiloi then penetrates the coral's epidermis, multiplies, and produces both heat-stable and heat-sensitive toxins, which affect zooxanthellae by inhibiting photosynthesis and causing lysis.
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In 1414 he died at Ardee, County Louth, Ireland, after being satirised by the O'Higgins' of Meath for despoiling the lands and raiding the cows of Niall O'Higgins. He lasted but five weeks, according to the Four Masters, before succumbing "to the virulence of the lampoons". His body was returned to his home at Lathom and was buried at Burscough Priory near Ormskirk, about 3 miles south-west of Lathom. This was deemed in some quarters the second such "Poet's Miracle" performed by the O'Higgins.
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Awareness of EAEC was increased by a serious outbreak in Germany during 2011, causing over 5000 cases and at least 50 fatalities. The pathogen responsible was found to be an EAEC O104:H4 strain which was lysogenized by a Shiga toxin encoding phage (typically associated with Shiga toxin-producing Escherichia coli, which often encode the adhesin intimin). The putative cause of the outbreak were sprouted fenugreek seeds. Strains of EAEC are highly genetically heterogeneous, and the identification of virulence factors important for pathogenesis has proven difficult.
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Elo researched the virulence and pathogenetic capacities of E.coli bacteria in 1950´s and human blood group antigens present in mushrooms. He qualified as surgeon 1961. He specialized in pediatric urology as the first MD in Finland, and has developed this branch essentially both in practice and by teaching, as even the general pediatric surgery in Finland in fact began systematically only in 1940s. He taught it as the docent in Helsinki University 1983-92, being the first teacher of pediatric urology in Finland.
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Stewart's wilt can be a serious disease of many corn types, including: sweet, dent, flint, flower, and popcorn. Sweet corn and popcorn cultivars are more susceptible to Stewart's wilt than field (dent) corn, but some dent corn inbreds and hybrids are susceptible. The production of virulence factor can be caused by the communication system between the bacteria known as quorum sensing. Stewart's wilt causes yield reductions by decreasing the size of corn stand or by limiting its production, resulting in fewer and smaller ears of corn.
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The 3′ UTR of mRNA hilD, a master regulator of Salmonella pathogenicity island 1 (SPI-1), is a prokaryotic example of functional 3'UTR. The 3'UTR is a target for hilD mRNA degradation by the degradosome and it may play a role in hilD and SPI-1 expression by serving as a target for the Hfq RNA chaperone. Under non-invasive conditions it is necessary to keep low levels of SPI-1 expression. It plays a role in S. Typhimurium virulence as a regulatory motif.
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Type VI secretion systems (T6SS) were discovered by the team of John Mekalanos at the Harvard Medical School in 2006 from Vibrio cholerae and Pseudomonas aeruginosa. They were recognised when mutations in the Vibrio Cholerae Hcp and VrgG genes caused diminished virulence and pathogenicity. In addition to their classic role as the pathogenicity factor, T6SS are also involved in defense against simple eukaryotic predators and in inter-bacteria interactions. The gene for T6SS form a gene cluster that consists of more than 15 genes.
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3D structure of pneumolysin Pneumolysin is a putative virulence factor of the Gram-positive bacteria Streptococcus pneumoniae. It is a pore-forming toxin of 53 kDa composed of 471 amino acids. It has a range of biological activity, including the ability to lyse and interfere with the function of cells and soluble molecules of the immune system. Released pneumolysin will aid the bacteria during colonization, by facilitating adherence to the host, during invasion by damaging host cells, and during infection by interfering with the host immune response.
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The Bäumler lab studies the human disease manifestations associated with Salmonella serotypes such as typhoid fever caused by Salmonella typhi and gastroenteritis caused by non-typhoidal Salmonella serotypes (e.g. S. Typhimurium). One focus of Dr. Bäumler's research is to understand why typhoid fever and gastroenteritis differ in the host response elicited at the site where both infections originate, the intestinal mucosa. The Bäumler lab aims to understand what Salmonella virulence factors and host factors contribute to the different disease manifestations caused by different serotypes of Salmonella.
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Characterization of the RRNPP family of quorum sensing regulators (which stands for proteins Rap, NprR, PrgX, PlcRd) were used in comparisons with RopB to postulate its structural functions. The Rap protein derived from Bacilli regulates sporulation, the NprR protein in Bacillus thuringiensis regulates necrotrophism, the PrgX protein regulates conjugation in Enterococcus faecalis, and PlcR protein regulates transcription of virulence factors in both Bacullis thuringiensis and Bacillus cereus. Similarities were observed in conserved asparagine residues on the TPR motifs of each of these proteins and in RopB.
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Orientia tsutsugamushi is a diverse species of bacteria. Ida A. Bengtson of the United States Public Health Service was the first to note the existence of different strains using antigen-antibody interaction (complement fixation test) in 1944. She observed that different strains had varying degree of virulence, and that the antibodies in the blood sera of patients cross- react to different strains. By 1946, she established that there were three principal strains (serotypes), namely Karp (from New Guinea), Gilliam (from India) and Seerangay (from British Malaya).
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Scanning electron micrograph of Mycobacterium tuberculosis A large quantity of cord factor is found in virulent M. tuberculosis, but not in avirulent M. tuberculosis. Furthermore, M. tuberculosis loses its virulence if its ability to produce cord factor molecules is compromised. Consequently, when all lipids are removed from the exterior of M. tuberculosis cells, the survival of the bacteria is reduced within a host. When cord factor is added back to those cells, M. tuberculosis survives at a rate similar to that of its original state.
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When George Nassau Clavering, Third Earl Cowper, died at Florence on 22 December 1789, his character was assailed with virulence in The World. Topham was indicted for libel, and the case was tried before Buller, who pronounced the articles to have been published with intent to throw scandal on the peer's family and as tending to a breach of the peace. The proprietor was found guilty. Counsel moved for an arrest of judgment on the ground of the misdirection of the judge to the jury.
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The body’s capability to react to antigens depends on a person's age, antigen type, maternal factors and the area where the antigen is presented. Neonates are said to be in a state of physiological immunodeficiency, because both their innate and adaptive immunological responses are greatly suppressed. Once born, a child’s immune system responds favorably to protein antigens while not as well to glycoproteins and polysaccharides. In fact, many of the infections acquired by neonates are caused by low virulence organisms like Staphylococcus and Pseudomonas.
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Having observed that most actinomycetales are saprophytes, that is able to survive outside of living organisms, with the help of a veterinary, Camille Guerin, he attempted to create a special nutritious environment for the bacillus that, in time, altered its features by eliminating the virulence and leaving only the antigenic power. Both of the scientist knew that this arduous task would require a lot of effort and time, because it was necessary to act on a large number of generations to change the genetic foundation of a species, nevertheless the velocity of the bacteria's reproduction allowed, since it was constantly monitored, to interfere with an important phase of its evolution. The environment deemed appropriate for the denaturation of the Mycobacterium bovis was a compost of potatoes cooked in the bile of an ox treated with glycerine, and Calmette re-inseminated it every three weeks for thirteen years, while checking for an enfeeblement of the pathogenic power of the bacillus. Having finally lost completely its virulence, the bovine tuberculosis germ grown with their method was the principal prophylactic weapon against human tuberculosis, and it helped to reduce considerably the frequency of this disease.
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Stuart Curran claims that the series "return the sonnet to its assumption of public and polemical responsibilities, an area conspicuously identified in the British tradition with the achievement of Milton [...] Most remarkable in the series, both for its rhetoric and its political daring, is the sonnet on Prime Minister Pitt. Suddenly appearing halfway through the series [...] it recaptures accents that had not [...] been heard in this form since Milton's 'On the New Forcers of Conscience' a century and a half before; nor did even Milton, for all his intensity, stretch his metaphors to such virulence".
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However, the move to the German capital was caused as much by the greater opportunities for publishing there as by his "Germanic" tendencies. Indeed, the increasing virulence of antisemitism in Germany meant that later on he had difficulty placing pieces which were felt to be too pro-Jewish—which was often another way of saying "not sufficiently anti-Jewish". Ehrengrab in Weißensee Cemetery More and more under Jew-hatred attacks, Franzos suffering from heart trouble died at the age of 55 in Berlin, where he is buried in the Weißensee Cemetery.
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The research goal on bacterial panicle blight is to develop effective disease control methods based on better understanding of the bacterial virulence mechanism and the rice defense system. To achieve this goal, LSU AgCenter scientists are conducting several different areas of research. First, scientists are making efforts to develop new rice varieties and lines resistant to bacterial panicle blight through conventional breeding and line development processes. More than 15,000 lines are evaluated annually to select promising lines showing high levels of disease resistance to bacterial panicle blight and other good agronomic traits.
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Infection with parasites can induce phenotypic plasticity as a means to compensate for the detrimental effects caused by parasitism. Commonly, invertebrates respond to parasitic castration or increased parasite virulence with fecundity compensation in order to increase their reproductive output, or fitness. For example, water fleas (Daphnia magna), exposed to microsporidian parasites produce more offspring in the early stages of exposure to compensate for future loss of reproductive success. A reduction in fecundity may also occur as a means of re-directing nutrients to an immune response, or to increase longevity of the host.
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He was born in Tarancón, New Castile, and joined the Dominican Order in Salamanca, where by 1546 he had succeeded Francisco de Vitoria to the theological chair in the university. A man of deep learning and originality, proud and a victim to the odium theologicum. His only rival was the gentle Bartolomé Carranza, also a Dominican and afterwards archbishop of Toledo. At the university the schools were divided between the partisans of the two professors; Cano pursued his rival with relentless virulence, and took part in the condemnation for heresy of his brother-friar.
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Fungi communicate in the phytobiome through chemical signaling to aid in sexual reproduction, sporulation, cell- to-cell recognition and antibiosis; however, only a fraction of these chemicals have been studied for their function. Mycorrhizal fungi establish symbiotic relationships with plants through the production of Myc factors, or chitooligosaccharides that are recognized by receptors in the plant. Nematode- trapping fungi often utilize fungal signaling molecules to initiate morphogensis towards prey. Other organisms can interfere with fungal signaling, such as plant-produced oxylipins that mimic fungal signaling molecules and can regulate fungal development or reduce virulence.
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In Europe during the late 1960s, it was found that a strain of C. parasitica was less virulent, only able to produce shallow cankers that the tree could eventually form callus tissue over. The trait of hypovirulence could be transferred from an avirulent strain to a lethal strain through anastomosis, the fusion of hyphae. It was later discovered that this attenuated virulence was due to infection by a dsRNA mycovirus, Cryphonectria hypovirus 1 (CHV1). Considering the nature of hypovirulent strains, there has been a strong interest to use them to manage lethal C. parasitica strains.
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S. aureus on trypticase soy agar: The strain is producing a yellow pigment staphyloxanthin. ;Staphylococcal pigments Some strains of S. aureus are capable of producing staphyloxanthin — a golden-coloured carotenoid pigment. This pigment acts as a virulence factor, primarily by being a bacterial antioxidant which helps the microbe evade the reactive oxygen species which the host immune system uses to kill pathogens. Mutant strains of S. aureus modified to lack staphyloxanthin are less likely to survive incubation with an oxidizing chemical, such as hydrogen peroxide, than pigmented strains.
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Invasion gene associated RNA (also known as InvR) is a small non-coding RNA involved in regulating one of the major outer cell membrane porin proteins in Salmonella species. InvR was originally predicted by computational screening the genome of Salmonella typhimurium for novel sRNA genes. In this screen 46 candidate sRNA genes not conserved in Escherichia coli were identified. The Salmonella the virulence factors that facilitate invasion of the host intestinal epithlium are located in a ~ 40 kb region in the Salmonella genome referred to as Salmonella pathogenicity Island 1 (SPI-1).
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Primary pulmonary EMZL (or primary pulmonary MALT lymphoma) is a rare disorder but nonetheless represents up to 80% of all lymphomas originating in the lung. The cause for developing this lymphoma is unclear. Some 16% of individuals with the disease present with features of an autoimmune disorder with one study reporting that 57 of 124 patients with the disorder evidenced Achromobacter xylosoxidans DNA in their lung lesions. Achromobacter xylosoxidans is a betaproteobacteria that is routinely isolated from the lungs of cystic fibrosis patients; it has a low virulence but is extremely resistant to antibiotics.
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There have been four secretion systems described in animal enteropathogens, such as Salmonella and Yersinia, with further sequence similarities in plant pathogens like Ralstonia and Erwinia. This is useful for further work with the YopR protein domain as comparative sequence and structure homology can be made. The type III secretion system is of great interest, as the YopR protein domain plays an important role. The type III secretion system transports virulence factors from the pathogen directly into the host cell when the bacterium is in close contact with the host.
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Thus, locals affiliated with the WLU, or not affiliated with the AFL, would be unable to join the local trades assembly. The DTA chose to punish not only those who found solidarity with a rival to the AFL, but also those whose loyalty to the AFL was judged insufficient. Miners Magazine, the publication of the WFM, accused the DTA of aiding the "increasing virulence" of the "rule or ruin policy of the paid agents" of the AFL. While the AFL leadership clearly encouraged such draconian rules, some Denver craft unions strongly supported the action.
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Unencapsulated strains are termed nontypable (NTHi) because they lack capsular serotypes; however, they can be classified by multilocus sequence typing. The pathogenesis of H. influenzae infections is not completely understood, although the presence of the capsule in encapsulated type b (Hib), a serotype causing conditions such as epiglottitis, is known to be a major factor in virulence. Their capsule allows them to resist phagocytosis and complement-mediated lysis in the nonimmune host. The unencapsulated strains are almost always less invasive; they can, however, produce an inflammatory response in humans, which can lead to many symptoms.
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Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis. This acts as an endotoxin and is responsible for septic shock and hemorrhage due to the destruction of red blood cells. Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response; fimbriae mediate attachment of the bacterium to the epithelial cells of the nasopharynx. It infects the cell by sticking to it mainly with long thin extensions called pili and the surface-exposed proteins Opa and Opc.
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Nature, May 17, 2009. By comparing the sequences of Listeria drawn from soil and drawn from the human gut, Cossart identified non-coding RNAs that contribute to Listeria's virulence, identified additional RNA repressors, and determined that riboswitches can act both downstream and upstream. As part of her work she has also developed important biological tools, including a transgenic mouse that was the first animal model to overcome bacterial species-specificity. The mouse carried a human version of a host cell membrane receptor that L. monocytogenes used to enter cells.
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While it is difficult to study P. chabaudi in its natural host given the difficulty of taming the thicket rat, it has been studied extensively in laboratory mice, largely using the clone P. chabaudi chabaudi (AS). The pathology resembles that of human malaria in that animals are susceptible to parasite growth and pathology such as anemia, hypoglycemia, changes in body temperature, weight loss, and occasional death. The other cloned strains vary in growth rates and virulence. One unique feature of this species is its prolonged course of infection.
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The Anopheles gambiae mosquito complex contains both species that are a vector for malaria and species that are not. Pests, species that cause diseases and their vectors, have direct importance for humans. When they are found to be cryptic species complexes, the ecology and the virulence of each of these species need to be re-evaluated to devise appropriate control strategies. Examples are cryptic species in the malaria vector genus of mosquito, Anopheles,the fungi causing cryptococcosis, and sister species of Bactrocera tyroni, or the Queensland fruit fly.
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It is not known whether the success of the inoculation technique used by Notions was due to its ability to decrease the virulence of the smallpox matter, or to the shallow intradermal insertion of the inoculant. The technique was highly successful and it and Notions were highly esteemed in Shetland. Notions was revered in contemporary accounts for the work he did. Reverend Andrew Dishington, the parish minister for Mid and South Yell, attested to the success of Notions' treatment: > Unassisted by education, and unfettered by the rules of art, he stands > unrivalled in this business.
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In the light of the virulence of the plague that had subsided seven years previously, Wycliffe's studies led him to the opinion that the close of the 14th century would mark the end of the world. While other writers viewed the plague as God's judgment on sinful people, Wycliffe saw it as an indictment of an unworthy clergy. The mortality rate among the clergy had been particularly high, and those who replaced them were, in his opinion, uneducated or generally disreputable. He was Master of Balliol College in 1361.
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While mortality among older conifers is less likely to occur, this does happen, however, in forests with dryer climates. The pathogenicity of Armillaria ostoyae appears to be more common in interior stands, but its virulence is seen to be greater in coastal conifers. Although conifers along the coastal regions show a lower rate of mortality against the root disease, infections can be much worse. Despite differences in how infections occur between these two regions, infections are generally established by rhizomorph strands, and pathogenicity is correlated to rhizomorph production.
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Bacterial effectors are proteins secreted by pathogenic bacteria into the cells of their host, usually using a type 3 secretion system (TTSS/T3SS), a type 4 secretion system (TFSS/T4SS) or a Type VI secretion system (T6SS). Some bacteria inject only a few effectors into their host’s cells while others may inject dozens or even hundreds. Effector proteins may have many different activities, but usually help the pathogen to invade host tissue, suppress its immune system, or otherwise help the pathogen to survive. Effector proteins are usually critical for virulence.
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Apophysomyces variabilis infections are not transmissible from person to person. Apophysomyces variabilis is one of four species in the genus Apophysomyces, which also includes A. elegans, A. ossiformis, and A. trapeziformis. In the past, Apophysomyces elegans was believed to be the species responsible for most cases of cutaneous mucormycosis attributed to Apophysomyces, but recently, some of the other species have been shown to be important in human infection. Since the new species have only recently been recognized, much remains to be learned about their relative clinical importance, comparative virulence, epidemiology, and anti-fungal drug susceptibilities.
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These factors include hyaluronic acid being severely limited, strong competition between hyaluronic synthesis and cell growth, and lactic acid being the main by-product of fermentation; which also will inhibit the overall fermentation process. Since hyaluronic acid is important for the virulence of S. zooepidemicus, as well as a valuable commercial production, hyaluronic acid production is constantly trying to be increased in industry and within the organism. Commercial uses for hyaluronic acid include an ingredient in cosmetics, skin filler for anti-aging and lip injections, in viscosurgery, and a lubricating substance in arthritic joints.
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Pseudogymnoascus destructans demonstrating lipase activity on Rhodamine B agar. Under laboratory conditions, P. destructans has been shown to produce numerous enzymes including β-glucosidase, esterase/esterase lipase/lipase, leucine and valine arylamidase, N-acetyl-β- glucosaminidase, naphthol-AS-B1-phosphohydrolase, both acid and alkaline phosphatases, various proteinase, and urease, while testing negative for cystine arylamidase, α-chymotrypsin, alpha/beta-galactosidase, β-glucuronidase, α-fucosidase, α-mannosidase, and trypsin. Important dual virulence factors found in P. destructans and many other pathogenic fungi include urease, proteinase (aspartyll) and superoxide dismutase.
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Francisella tularensis is a pathogenic species of Gram-negative coccobacillus, an aerobic bacterium. It is nonspore-forming, nonmotile, and the causative agent of tularemia, the pneumonic form of which is often lethal without treatment. It is a fastidious, facultative intracellular bacterium, which requires cysteine for growth. Due to its low infectious dose, ease of spread by aerosol, and high virulence, F. tularensis is classified as a Tier 1 Select Agent by the U.S. government, along with other potential agents of bioterrorism such as Yersinia pestis, Bacillus anthracis, and Ebola virus.
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In 1563 the City of London was overcrowded, unsanitary, and poorly-policed. Queen Elizabeth reigned in her 5th year and the government struggled with a rapidly increasing population. Although sanitation was a constant problem, the city had gone over a dozen years without a plague epidemic and many contemporary Londoners were unconcerned about the disease. That changed in 1563 when plague suddenly erupted in Derby, Leicester, and London with such virulence that sickness spread to English troops garrisoned at Havre, weakening them and causing a surrender to French forces.
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Vibrio coralliilyticus is a causative agent of both bacterially induced coral bleaching and larval oyster mortality. In corals this bleaching is the result of the death of endosymbiont colonies which is mediated by V. coralliilyticus disabling Photosystem II and in some cases causing cell lysis. This also seems to be exacerbated by increased virulence as a result of increasing ocean temperatures. In oyster larvae an outbreak of V. coralliilyticus in a hatchery can result in mortality of up to 80%, greatly reducing hatchery production for that season leading to significant economic loss.
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Pathogens may be intentionally or unintentionally genetically modified to change their characteristics, including virulence or toxicity. When intentional, these mutations can serve to adapt the pathogen to a laboratory setting, understand the mechanism of transmission or pathogenesis, or in the development of therapeutics. Such mutations have also been used in the development of biological weapons, and dual-use risk continues to be a concern in the research of pathogens. The greatest concern is frequently associated with gain of function mutations, which confer novel or increased functionality, and the risk of their release.
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More serious was the opposition of the sons of Michael of Epirus, Nikephoros I Komnenos Doukas and his half- brother John the Bastard: they posed as the defenders of Orthodoxy and gave support to the anti-unionists fleeing Constantinople. Michael at first responded with comparative leniency, hoping to win the anti-unionists through persuasion, but eventually the virulence of the protests led him to resort to force. Many anti-unionists were blinded or exiled. Two prominent monks, Meletios and Ignatios, were punished: the first had his tongue cut out, the second was blinded.
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Some research suggests that M. africanum is adapted to west African populations. M. africanum may be being outcompeted by other Mtb lineages in other regions; however, genetic studies have found no difference in the number of virulence genes or genetic diversity between M. tuberculosis and M. africanum. No animal reservoir has been identified for Mycobacterium africanum despite having been found various wild animals. It has a similar degree of infectivity to the regular M. tuberculosis organism but is less likely to progress to clinical disease in an immunocompetent individual.
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The first way is reversible; many bacteria like Salmonella have two proteins to turn the GTPases on and off. The other process is irreversible, using toxins to completely change the target GTPase and shut down or override gene expression. One example of a bacterial virulence factor acting like a eukaryotic protein is Salmonella protein SopE it acts as a GEF, turning the GTPase on to create more GTP. It does not modify anything, but overdrives normal cellular internalization process, making it easier for the Bacteria to be colonized within a host cell.
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In his nightly radio broadcasts, Bose spoke with increasing virulence against Gandhi, who had been released from jail in 1944, and was engaged in talks with British administrators, envoys and Muslim League leaders. Some senior INA officers began to feel frustrated or disillusioned with Bose and to prepare quietly for the arrival of the British and its consequences. During the first two weeks of August 1945, events began to unfold rapidly. With the British threatening to invade Malaya and with daily American aerial bombings, Bose's presence in Singapore became riskier by the day.
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Prophages are able to do a multitude of things within their respective bacterial strains. Prophages can increase the virulence potential of bacterial strains in both humans and plant pathogens as well as increase the ability of the bacteria to survive in harsh environments. Pathogens have been able to adapt and thrive in a wide range of environments. Some anaerobic pathogens such as Clostridium perfringens and Clostridium difficile exist in the intestines and are unable to survive in places with large amounts of oxygen for extended periods of time.
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Another class of plant disease resistance genes opens a “trap door” that quickly kills invaded cells, stopping pathogen proliferation. Xanthomonas and Ralstonia transcription activator–like (TAL) effectors are DNA-binding proteins that activate host gene expression to enhance pathogen virulence. Both the rice and pepper lineages independently evolved TAL-effector binding sites that instead act as an executioner that induces hypersensitive host cell death when up- regulated. Xa27 from rice and Bs3 and Bs4c from pepper, are such “executor” (or "executioner") genes that encode non-homologous plant proteins of unknown function.
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Trypanothione allows the parasites to fend off free radicals and other toxic oxidants produced by the immune system of the infected patient, and was shown to be vital for parasite survival and virulence. For instance, antimonials neutralize the Leishmania parasite's antioxidant defence system, allowing the patient to clear the infection. Studies on the effect of drugs on trypanothione metabolism resulted in the discovery that fexinidazole is a potential oral treatment for visceral leishmaniasis. Since 2006, Alan Fairlamb and Mike Ferguson have been co-directors of the Drug Discovery Unit at the University of Dundee.
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With the exception of smallpox, most pandemics are caused by newly evolved viruses. These "emergent" viruses are usually mutants of less harmful viruses that have circulated previously either in humans or other animals. Severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) are caused by new types of coronaviruses. Other coronaviruses are known to cause mild infections in humans, so the virulence and rapid spread of SARS infections—that by July 2003 had caused around 8,000 cases and 800 deaths—was unexpected and most countries were not prepared.
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Some patients even have health conditions as serious as tumors, infected joint cavities and collapsed lungs. Within those infected, P. stutzeri strains have been isolated from the blood, feces, cerebral spinal fluid, ears, eyes, and organ systems (such as respiratory and urinary). When strains of this bacterium are discovered within infected patients they are often accompanied by other pathogenic microbes. While P. stutzeri has caused numerous infections since it has been discovered, it has caused few deaths, giving it a much lower virulence rating in relation to other Pseudomonas species, such as Pseudomonas aeruginosa.
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Enterococcus faecium is a Gram-positive sphereically-shaped (coccus) bacteria that tends to occur in pairs or chains, most commonly involved in HAI in immunocompromised patients. It often exhibits a resistance to β-lactam antibiotics including penicillin and other last resort antibiotics. There has also been a rise in vancomycin resistant enterococci (VRE) strains, including an increase in E. faecium resistance to vancomycin, particularly vancomycin-A. These vancomycin- resistant strains display a profound ability to develop and share their resistance through horizontal gene transfer, as well as code for virulence factors that control phenotypes.
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Studies on the pathogenesis of C. jejuni show that for this organism to cause disease, the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection, the organism must penetrate the gastrointestinal mucus, which it does using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and can then induce diarrhea by toxin release.
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Hypoacylated lipopolysaccharide (LPS) from C. jejuni induces moderate TLR4-mediated inflammatory response in macrophages and such LPS bioactivity may eventually result in the failure of local and systemic bacterial clearance in patients. At the same time, moderation of anti-bacterial responses may be advantageous for infected patients in clinical practice, since such an attenuated LPS may not be able to induce severe sepsis in susceptible individuals. One of the most important virulence factor of C. jejuni are flagella. The flagellar protein FlaA has been proven to be one of the abundant proteins in the cell.
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Even though plants do not have cells that can move and fight foreign organisms and they do not have a somatic adaptive immune system, they do have and depend on innate immunity of each cell and on systemic signals. In responses to infections, plants have a two-branched innate immune system. The first branch has to recognize and respond to molecules that are similar to classes of microbes, this includes non-pathogens. On the other hand, the second branch responds to pathogen virulence factors, either directly or indirectly to the host.
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Factors such as age or genetic differences between individuals, the level of virulence of the individual strain of virus, as well as exogenous influences such as co-infection with other microbes may determine the rate and severity of HIV disease expression. Similarly, some people infected with hepatitis B, for example, show no symptoms or only jaundice and clear their infection, while others suffer disease ranging from chronic liver inflammation to cirrhosis and hepatocellular carcinoma. Co-factors probably also determine why some smokers develop lung cancer while others do not.
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DNA adenine methylation is important in bacteria virulence in organisms such as Escherichia coli, Salmonella, Vibrio, Yersinia, Haemophilus, and Brucella. In Alphaproteobacteria, methylation of adenine regulates the cell cycle and couples gene transcription to DNA replication. In Gammaproteobacteria, adenine methylation provides signals for DNA replication, chromosome segregation, mismatch repair, packaging of bacteriophage, transposase activity and regulation of gene expression. There exists a genetic switch controlling Streptococcus pneumoniae (the pneumococcus) that allows the bacterium to randomly change its characteristics into six alternative states that could pave the way to improved vaccines.
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For humans and other complex organisms, this process is best characterized by the digestive system which breaks down solid food via exoenzymes. The small molecules, generated by the exoenzyme activity, enter into cells and are utilized for various cellular functions. Bacteria and fungi also produce exoenzymes to digest nutrients in their environment, and these organisms can be used to conduct laboratory assays to identify the presence and function of such exoenzymes. Some pathogenic species also use exoenzymes as virulence factors to assist in the spread of these disease-causing microorganisms.
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SEM of Clostridioides difficile bacteria PaLoc Reference: Clostridioides difficile strain 630, DSM 27543, genome GenBank accession number AM180355 Positions 770.154 to 789.973 bp, total locus size 19.8 kb. Clostridium difficile toxin A (TcdA) is a toxin generated by Clostridioides difficile, formerly known as Clostridium difficile. It is similar to Clostridium difficile Toxin B. The toxins are the main virulence factors produced by the gram positive, anaerobic, Clostridioides difficile bacteria. The toxins function by damaging the intestinal mucosa and cause the symptoms of C. difficile infection, including pseudomembranous colitis.
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Clouser works with Dr. Louis Mansky and Dr. Steven Patterson to investigate antiviral properties of ribonucleoside and nucleoside analogues against the human immunodeficiency virus. In their laboratory model system, two nucleoside analogues, decitabine and gemcitabine, have been found to cause lethal mutagenesis of the HIV-1 virus when used combination therapy. These two drugs are FDA approved and used interventionally as chemotherapy drugs. When used together, they have been found to have strong antiviral properties against HIV-1 by causing the virus to rapidly mutate, lose virulence factors, and become non-infectious.
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This includes clinically important bacteria such as Mycobacteria which have a thick peptidoglycan cell wall like a Gram-positive bacterium, but also a second outer layer of lipids. In many bacteria, an S-layer of rigidly arrayed protein molecules covers the outside of the cell. This layer provides chemical and physical protection for the cell surface and can act as a macromolecular diffusion barrier. S-layers have diverse but mostly poorly understood functions, but are known to act as virulence factors in Campylobacter and contain surface enzymes in Bacillus stearothermophilus.
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In fish, the incubation period of L. garvieae is very brief and the microorganism performs with high virulence. In an experimental infection by intraperitoneal route in Japanese yellowtail, it caused symptoms 2–3 days post-inoculation, while intramuscular infection in grey mullet (Mugil cephalus) produced its first symptoms and fatalities two days post-inoculation. Correspondingly, intraperitoneal experimental infection in rainbow trout caused the first symptoms and deaths three days post-inoculation. The gross pathology of lactococcosis arises with the presence of a rapid and general anorexia, melanosis, lethargy, loss of orientation, and irregular swimming.
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Typhus appeared again in the late 1830s, and between 1846 and 1849 during the Great Irish Famine. Spreading to England, and called "Irish fever", it was noted for its virulence. It killed people of all social classes, as lice were endemic and inescapable, but it hit particularly hard in the lower or "unwashed" social strata. In Canada alone, the typhus epidemic of 1847 killed more than 20,000 people from 1847 to 1848, mainly Irish immigrants in fever sheds and other forms of quarantine, who had contracted the disease aboard coffin ships.
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A lysogen or lysogenic bacterium is a bacterial cell which can produce and transfer the ability to produce a phage. A prophage is either integrated into the host bacteria's chromosome or more rarely exists as a stable plasmid within the host cell. The prophage expresses gene(s) that repress the phage's lytic action, until this repression is disrupted (see lytic cycle). Currently a variety of studies are being conducted to see whether other genes are active during lysogeny, examples of which include phage-encoded tRNA and virulence genes.
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When a pathogen is sensed, the ADP is exchanged for Adenosine triphosphate (ATP) and this induces a conformational change in the NLR protein, which results in HR. At the N-terminus, the NLR either has a Toll-Interleukin receptor (TIR) domain (also found in mammalian toll-like receptors) or a coiled-coil (CC) motif. Both TIR and CC domains are implicated in causing cell death during HR. The C-terminus of the NLRs consists of a leucine-rich repeat (LRR) motif, which is involved in sensing the pathogen virulence factors.
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Recent structural studies of CC-NLR proteins have suggested that after the virulence factors are sensed, the NLRs assemble into a pentameric structure known as the resistosome. The resistosome seems to have a high affinity for the cellular membrane. When the resistosome is assembled, a helix sticks out from the N-terminus of each NLR and this creates a pore in the membrane which allows leakage of ions to occur and thus the cell dies. However, this mechanism is only inferred from the structure and there are currently no mechanistic studies to support this.
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These "emergent" viruses are usually mutants of less harmful viruses that have circulated previously either in humans or in other animals. Severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) are caused by new types of coronaviruses. Other coronaviruses are known to cause mild infections in humans, so the virulence and rapid spread of SARS infections—that by July 2003 had caused around 8,000 cases and 800 deaths—was unexpected and most countries were not prepared. A related coronavirus emerged in Wuhan, China in November 2019 and spread rapidly around the world.
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His biographer, Hans Trefousse, suggested that another reason for Stevens's virulence was an attack of disease in the late 1820s that cost him his hair (he thereafter wore wigs, often ill-fitting), and "the unwelcome illness may well have contributed to his unreasonable fanaticism concerning the Masons."Trefousse, pp. 25–26 By 1829, Anti-Masonry had evolved into a political party, the Anti-Masonic Party, that proved popular in rural central Pennsylvania. Stevens quickly became prominent in the movement, attending the party's first two national conventions in 1830 and 1831.
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Specifically, animal models indicate that the transcriptional profile of the pathogen changes as it prepares to enter an aquatic environment. This transcriptional change results in a loss of ability of V. cholerae to be cultured on standard media, a phenotype referred to as 'viable but non-culturable' (VBNC) or more conservatively 'active but non- culturable' (ABNC). One study indicates that the culturability of V. cholerae drops 90% within 24 hours of entering the water, and furthermore that this loss in culturability is associated with a loss in virulence. Both toxic and non-toxic strains exist.
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This discovery suggests the possibility that P2 and P3 could be used as a biological control agent when other methods do not work. A mite associated with pineapples, Steneotarsonemus ananas Tryon also benefits P. funiculosum. Although this mite is not a vector for the pathogen, there is an association between it and pineapple disease in which the mite increases the virulence of P. funiculosum by creating wounds through which P. funiculosum enters the plantRohrbach, K. G., and D. J. Phillips. “Postharvest Diseases Of Pineapple.” Acta Horticulturae, no. 269, 1990, pp. 503–508.
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Along the way, the different civil rights groups struggled to reconcile their goals and to enhance the meaning of the march to promote black freedoms. It grew slowly and was embraced by black communities along the way, and by some sympathetic whites. Other whites expressed hostility, jeering and threatening, driving close to marchers. Although overt violence was generally limited, marchers from out of state were shocked and horrified by the virulence of hate expressed in some communities, particularly Philadelphia, where three civil rights workers had been murdered in 1963, and Canton.
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At Oblensk, Popov and his team spliced the diphtheria toxin gene into the plague bacterium, thus creating a highly virulent and deadly strain. Popov has described Biopreparat's "Project Bonfire", whose goal was to develop antibiotic-resistant microbial strains, and "Project Factor", whose goal was to create microbial weapons with new biologic properties that would result in high virulence, improved stability, and new clinical syndromes.Popov, S (2000), "Interview: Serguei Popov" , J Homeland Security, 13 November 2000; Accessed on 1 May 2011. In 1992, Popov defected to the United Kingdom and later traveled to the United States.
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Elaine Tuomanen received her M.D. from McGill University. She is a member of the Association of American Physicians and a Fellow of the American Academy for Microbiology. At St. Jude’s Research Hospital, she focuses on the pathogenesis of infectious diseases in children, which can be seen in her initiatives of the Children’s GMP Manufacturing Facility and the Translational Trials Unit. Among her influential contributions are studies that link pneumococcal virulence factors to specific host receptors, the inflammatory bioactivities of cell wall, and the increased susceptibility of children with sickle cell disease to pneumococcal disease.
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Pseudomonas sRNA are non-coding RNAs (ncRNA) that were predicted by the bioinformatic program SRNApredict2. This program identifies putative sRNAs by searching for co-localization of genetic features commonly associated with sRNA-encoding genes and the expression of the predicted sRNAs was subsequently confirmed by Northern blot analysis. These sRNAs have been shown to be conserved across several pseudomonas species but their function is yet to be determined. Using Tet-Trap genetic approach RNAT genes post-transcriptionally regulated by temperature upshift were identified: ptxS (implicated in virulence) and PA5194.
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Waxworms can replace mammals in certain types of scientific experiments with animal testing, especially in studies examining the virulence mechanisms of bacterial and fungal pathogens. Waxworms prove valuable in such studies because the innate immune system of insects is strikingly similar to that of mammals. Waxworms survive well at human body temperature and are large enough in size to allow straightforward handling and accurate dosing. Additionally, the considerable cost savings when using waxworms instead of small mammals (usually mice, hamsters, or guinea pigs) allows testing throughput that is otherwise impossible.
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This line of descent includes Earth life, which however descends from a genetically- damaged branch in which the quantum link has been broken. The emergent intelligence cherishes the sentient life that occasionally evolves on its worlds, and regrets that is cannot communicate with humans or control the virulence of the Isian biome. Zoe, her lover, and - it is implied - all the humans who had died after being infected by Isis are "remembered" by the super-organism, in a sense living forever within the immortal quantum "cloud." The remaining ground stations fail one by one.
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The CsrB RNA is a non-coding RNA that binds to approximately 9 to 10 dimers of the CsrA protein. The CsrB RNAs contain a conserved motif CAGGXXG that is found in up to 18 copies and has been suggested to bind CsrA. The Csr regulatory system has a strong negative regulatory effect on glycogen biosynthesis, glyconeogenesis and glycogen catabolism and a positive regulatory effect on glycolysis. In other bacteria such as Erwinia carotovora the RsmA protein has been shown to regulate the production of virulence determinants, such extracellular enzymes.
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Apicystis bombi, a pathogenic protozoan, has been recently found in Bombus ruderatus species in Argentina. Apicystis bombi can have many negative effects in bee populations due to it high virulence, its generalism for many different bumblebee species, and its ability to affect both commercially produced and native born colonies. Apicystis bombi can cause extreme physical and behavior effects within colonies, along with inhibiting colony foundation, both of which increase mortality. This parasite is thought to have been contracted in B. ruderatus due to the interaction with another invasive species, Bombus terrestris.
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Dr. Aballay's laboratory takes advantage of the compromise between complexity and tractability of the C. elegans–S. enterica pathogenesis model. The focus of the laboratory is to use C. elegans as a host to screen thousands of bacterial clones from mutagenized libraries to identify novel Salmonella virulence factors and to address how they alter host signaling pathways. Since several components of innate immunity are conserved among different organisms throughout evolution, his group is also exploiting the genetic and genomic resources available for C. elegans to study the basis of the immune response.
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The changes included making pasteurization standard and greatly tightening the standards of cleanliness in milkhouses on dairy farms. The expense prompted delay and skepticism in the industry, but the new hygiene rules eventually became the norm. Although these measures have sometimes struck people as overdone in the decades since, being unhygienic at milking time or in the milkhouse, or drinking raw milk, are not a safe alternative. In the decades after Evans's work, this genus, which received the name Brucella in honor of Bruce, was found to contain several species with varying virulence.
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These variants correspond to the two known PAI variants. Aside from the T3SS, two genes encoding well-characterized virulence proteins are typically found on the PAI, the thermostable direct hemolysin gene (tdh) and/or the tdh-related hemolysin gene (trh). Strains possessing one or both of these hemolysins exhibit beta- hemolysis on blood agar plates. A distinct correlation seems to exist between presence of tdh, trh, and the two known T3SS variants: observations have shown T3SS2α correlating with tdh+/trh- strains, while T3SS2β correlates with tdh-/trh+ strains.
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Solid squares show the appearance of a new strain, causing recurring influenza pandemics. Broken lines indicate uncertain strain identifications. The first significant step towards preventing influenza was the development in 1944 of a killed-virus vaccine for influenza by Thomas Francis, Jr. This built on work by Australian Frank Macfarlane Burnet, who showed that the virus lost virulence when it was cultured in fertilized hen's eggs. Application of this observation by Francis allowed his group of researchers at the University of Michigan to develop the first influenza vaccine, with support from the U.S. Army.
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In summary, rhamnolipids have been shown unequivocally to be a potent virulence factor in the human host, however, they are also produced outside of the host, for example in a soil environment. Rhamnolipids contribute to the establishment and maintenance of infection in cystic fibrosis patients in a number of ways, they disrupt the bronchial epithelium by disrupting the cell membranes, which promotes paracellular invasion of Pseudomonas aeruginosa and causes ciliostasis, further preventing the clearing of mucus. They also solubilise lung surfactant, allowing phospholipase C access to cell membranes and are necessary for correct biofilm formation.
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Although its intracellular function has not been elucidated, apoL1 circulating in plasma has the ability to kill the trypanosome Trypanosoma brucei that causes sleeping sickness. Recently, two coding sequence variants in APOL1 have been shown to associate with kidney disease in a recessive fashion while at the same time conferring resistance against Trypanosoma brucei rhodesiense. This resistance is due, in part, to decreased binding of the G1 and G2 APOL1 variants to the T. b. rhodesiense virulence factor, serum resistance-associated protein (SRA) as a result of the C-terminal polymorphisms.
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Under positive parasite interactions, disease transmission and progression are enhanced and this is also known as syndemism. Negative parasite interactions include microbial interference when one bacterial species suppresses the virulence or colonisation of other bacteria, such as Pseudomonas aeruginosa suppressing pathogenic Staphylococcus aureus colony formation. The general patterns of ecological interactions between parasite species are unknown, even among common coinfections such as those between sexually transmitted infections. However, network analysis of a food web of coinfection in humans suggests that there is greater potential for interactions via shared food sources than via the immune system.
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A two-component system, involving histidine kinase and a variable response regulator protein, may be critical to the virulence of some fungal strains such as Candida albicans, which is often responsible for causing candidiasis in immunocompromised persons. C. albicans with a deletion of CHK1, the two-component histidine kinase gene, show defects in morphogenesis and a drastic decrease in the cell’s ability to resist elimination by human neutrophils. As humans lack this two-component system, it may be a good target for anti-microbial agents in order to treat candidiasis.
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One member of the MVF family, MviN (TC# 2.A.66.4.1) of Salmonella typhimurium, has been shown to be an important virulence factor for this organism when infecting the mouse. In several bacteria, mviN genes occur in operons including glnD genes that encode the uridyl transferase that participates in the regulation of nitrogen metabolism. It is thought that MviN may flip the Lipid II peptidoglycan (PG) precursor from the cytoplasmic side of the inner membrane to the periplasmic surface acting as a putative lipid flippase in Salmonella typhimurium.
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N. meningitidis has a polysaccharide capsule that surrounds the outer membrane of the bacterium and protects against soluble immune effector mechanisms within the serum. It is considered to be an essential virulence factor for the bacteria. N. gonorrhoeae possesses no such capsule. Unlike most other Gram-negative bacteria, which possess lipopolysaccharide (LPS), both pathogenic and commensal species of Neisseria have a lipooligosaccharide (LOS) which consists of a core polysaccharide and lipid A. It functions as an endotoxin, protects against antimicrobial peptides, and adheres to the asialoglycoprotein receptor on urethral epithelium.
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However, it has been reported that PTPN11/Shp2 can act as either tumor promoter or suppressor. In aged mouse model, hepatocyte-specific deletion of PTPN11/Shp2 promotes inflammatory signaling through the STAT3 pathway and hepatic inflammation/necrosis, resulting in regenerative hyperplasia and spontaneous development of tumors. Decreased PTPN11/Shp2 expression was detected in a subfraction of human hepatocellular carcinoma (HCC) specimens. The bacterium Helicobacter pylori has been associated with gastric cancer, and this is thought to be mediated in part by the interaction of its virulence factor CagA with SHP2.
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At the beginning of the outbreak, widespread panic regarding the virulence of the disease and the UN's denial of the blame caused increased tension between the UN and the Haitian community. On 15 November 2010, a riot broke out in Cap-Haïtien following the death of a young Haitian inside the Cap-Haïtien UN base and rumours that the outbreak was caused by UN soldiers from Nepal. Protesters demanded that the Nepalese brigade of the UN leave the country. At least 5 people were killed in the riots, including 1 UN personnel.
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The virus has a 151-kbp genome, consisting of a central coding region which is bounded by identical 2.4 kbp-inverted terminal repeats and contains 156 genes. There are 146 conserved genes when comparing LSDV with chordopoxviruses of other genera. These genes encode proteins which are involved in transcription and mRNA biogenesis, nucleotide metabolism, DNA replication, protein processing, virion structure and assembly, and viral virulence and host range. Within the central genomic region, LSDV genes share a high degree of collinearity and amino acid identity with the genes of other mammalian poxviruses.
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Before the MINUSTAH troops from Nepal were sent to Haiti, a cholera outbreak had just occurred in Nepal. In the original research to trace the origin of the outbreak, the Nepal strains were not available. Phylodynamic analyses were performed on the Haitian strain and the Nepalese strain when it became available and affirmed that the Haitian cholera strain was the most similar to the Nepalese cholera strain. This outbreak strain of cholera in Haiti showed signs of an altered or hybrid strain of V. cholerae associated with high virulence.
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This can result in changes in red cell membranes, including translocation of phosphatidylserine to their surface, followed by macrophage recognition and ingestion. The authors suggest that this mechanism is likely to occur earlier in abnormal than in normal red cells, thereby restricting multiplication in the former. In addition, binding of parasitized sickle cells to endothelial cells is significantly decreased because of an altered display of P. falciparum erythrocyte membrane protein-1 (PfMP-1). This protein is the parasite's main cytoadherence ligand and virulence factor on the cell surface.
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Cyclic di-GMP-II riboswitches (also c-di-GMP-II riboswitches) form a class of riboswitches that specifically bind cyclic di-GMP, a second messenger used in multiple bacterial processes such as virulence, motility and biofilm formation. Cyclic di-GMP II riboswitches are structurally unrelated to cyclic di-GMP-I riboswitches, though they have the same function. Cyclic di-GMP-II riboswitches were discovered by bioinformatics, and are common in species within the class Clostridia and the genus Deinococcus. They are also found in some other bacterial lineages.
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The Black Death killed three fourths of the European population, delaying progress and, ultimately, the Industrial Revolution. Most of Central Europe was conquered by the Ottoman Empire, which occupied it until the twentieth century, leaving it in no shape for colonization of much of the non- European world as in our timeline. Constantinople was conquered in 1420, the Ottomans moved into Vienna in 1440, and took over Paris in 1460, before invading the British Isles in 1490. The greater virulence of the Black Death in Europe allowed non-European powers to emerge.
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Within infected tissues, this yeast produces several enzymes such as proteinase, phospholipase, hyaluronidase and chondroitin-sulphatase. Proteinase and phospholipase are also released in infections involving Candida albicans and have been found to contribute to its virulence by inducing pores into host cell membranes, which eventually lead to their loss of function. For this reason it has been suggested that these enzymes may also serve a function in the pathogenicity of M. pachydermatis. However, pathogenicity in this species has yet to be associated with any specific genotypic and phenotypic traits.
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As of 2009, more than 20 different strains have been established in humans based on antigenic variation using serological tests such as complement fixation and immunofluorescence assay. The number is much higher if the strains in rodents and mites are taken into account. For example, a study in Japan in 1994 reported 32 strains, 14 from human patients, 12 from wild rodents, and 6 from trombiculid mites. The different strains exert different levels of virulence, and the most virulent is KN-3, which is predominant among wild rodents.
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Blautia obeum is a species of anaerobic, gram-positive bacteria found in the gut. It has been shown that B. obeum along with other relevant taxa play an important role both in the recovery process from V. cholerae infection and microbiota maturation in children. Moreover, experiments in model mice show that B. obeum strain AI-2 reduces the pathogenicity of V. cholerae. The data show that the expression of quorum sensing autoinducers by B. obeum is increased in V. cholera infections and they repress the expression of several V. cholera virulence factors.
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Populations of M. ovipneumoniae of infected sheep are often found to have varying strains of the bacterium within one animal, but the different strains vary in virulence. The bacterium can be found within the lungs, trachea, and nasal cavity of small ruminants. However, the detection of M. ovipneumoniae can be obtained by bacteriologic culture, molecular diagnostics, and serology, allowing for the bacterium to be grown in culture, species- specific DNA sequences, and specific antibiodies identified, respectivitly. In July 2007, this species of Mycoplasma was linked to the deaths of bighorn sheep in the Western United States.
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Riitta Johanna Mappes (born 13 October 1965 in Valkeakoski, Finland) is a Finnish evolutionary ecologist. In her research, Mappes focuses on interspecific interactions, especially the evolution of warning signals and mimicry in chemically defended prey, as well as on the evolution of bacterial virulence and the evolution of sexual and asexual reproduction. In 2003 The Academy of Finland awarded Mappes the 'Young Dynamic Researcher Award' for her research merits, especially for developing and using the ‘novel world method’ in studying the evolution of aposematism. Mappes earned her MSc degree in 1991 and her PhD in 1994 from the University of Jyväskylä, Finland.
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Invasive strains of non-typhoidal salmonella, such as Salmonella Typhimurium ST313 have recently been labelled as causing emerging diseases in Africa. Key host immune deficiencies associated with HIV, malaria and malnutrition have contributed to a wide spread of this disease and the need to use expensive antimicrobial drugs in the poorest health services in the world. But also bacterial factors, such as upregulated activity of the virulence gene pgtE, due to a single nucleotide polymorphism (SNP) in its promoter region, have been shown to have a great impact upon the pathogenesis of this particular Salmonella sequence type.
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In the specific case of topoisomerases, some bacteria have mutated one of their amino acids so that the ciprofloxacin can only create a weak bond to the topoisomerase. This is one of the methods that bacteria use to become resistant to antibiotics. Ciprofloxacin treatment can therefore potentially lead to the generation of mutations that may render bacteria resistant to ciprofloxacin. In addition, ciprofloxacin has also been shown to induce via the SOS response dissemination of virulence factors and antibiotic resistance determinants, as well as the activation of integron integrases, potentially increasing the likelihood of acquisition and dissemination of antibiotic resistance by bacteria.
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Response to light is important in pathogenicity of these bacteria and regulates surface attachment and production of biofilm. Xanthomonas possess almost all known secretion systems (types I to VI) that play different roles in the life and disease cycle, with type III secretion system (T3SS) being the key factor of pathogenicity. Typically, Xanthomonas T3SS injects a cocktail of 20-30 effector proteins that interfere with plant immune system and various host cellular processes. Many of the effectors are presumably redundant as individual deletions of effector genes does not impair virulence, however mutations in T3SS apparatus has strong effect.
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Panton–Valentine leukocidin (PVL) is one of many toxins associated with S. aureus infection. Because it can be found in virtually all CA-MRSA strains that cause soft-tissue infections, it was long described as a key virulence factor, allowing the bacteria to target and kill specific white blood cells known as neutrophils. This view was challenged, however, when it was shown that removal of PVL from the two major epidemic CA- MRSA strains resulted in no loss of infectivity or destruction of neutrophils in a mouse model.MRSA Toxin Acquitted: Study Clears Suspected Key to Severe Bacterial Illness , NIH news release, Nov.
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Most vaccines consist of viruses that have been attenuated, disabled, weakened or killed in some way so that their virulent properties are no longer effective. Genetic engineering could theoretically be used to create viruses with the virulent genes removed. This does not affect the viruses infectivity, invokes a natural immune response and there is no chance that they will regain their virulence function, which can occur with some other vaccines. As such they are generally considered safer and more efficient than conventional vaccines, although concerns remain over non-target infection, potential side effects and horizontal gene transfer to other viruses.
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Vitamin C deficiency causes scurvy, a serious and painful disease in which defective collagen prevents the formation of strong connective tissue. Gums deteriorate and bleed, with loss of teeth; skin discolors, and wounds do not heal. Prior to the 18th century, this condition was notorious among long-duration military, particularly naval, expeditions during which participants were deprived of foods containing vitamin C. An autoimmune disease such as lupus erythematosus or rheumatoid arthritis may attack healthy collagen fibers. Many bacteria and viruses secrete virulence factors, such as the enzyme collagenase, which destroys collagen or interferes with its production.
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Clostridium difficile, the causative agent of nosocomial antibiotic-associated diarrhea and pseudomembranous colitis, possesses two main virulence factors: the large clostridial cytotoxins A (TcdA; TC# 1.C.57.1.2) and B (TcdB, TC# 1.C.57.1.1). Action by large clostridial toxins (LCTs) from Clostridium difficile includes four steps: (1) receptor-mediated endocytosis, (2) translocation of a catalytic glucosyltransferase domain across the membrane, (3) release of the enzymatic part by auto-proteolysis, and (4) inactivation of Rho family proteins. Cleavage of toxin B and all other large clostridial cytotoxins, is an autocatalytic process dependent on host cytosolic inositolphosphate cofactors.
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It not only induces biofilm formation, but also increases virulence in pneumonia and meningitis. It has been proposed that competence development and biofilm formation is an adaptation of S. pneumoniae to survive the defenses of the host. In particular, the host's polymorphonuclear leukocytes produce an oxidative burst to defend against the invading bacteria, and this response can kill bacteria by damaging their DNA. Competent S. pneumoniae in a biofilm have the survival advantage that they can more easily take up transforming DNA from nearby cells in the biofilm to use for recombinational repair of oxidative damages in their DNA.
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