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Virulence
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{{Short description|Severity of disease pathogens on its host}} {{For|the academic journal|Virulence (journal)}} '''Virulence''' is a [[pathogen]]'s or [[microorganism]]'s ability to cause damage to a host. In most cases, especially in animal systems, virulence refers to the degree of damage caused by a microbe to its [[host (biology)|host]].<ref name="Pirofski2012">{{cite journal|vauthors=Pirofski LA, Casadevall A|title=Q and A: What is a pathogen? A question that begs the point|journal=BMC Biology|volume=10|pages=6|year=2012|pmid=22293325|pmc=3269390|doi=10.1186/1741-7007-10-6 |doi-access=free }}</ref> The [[Pathogen#Pathogenicity|pathogenicity]] of an organism—its ability to cause [[disease]]—is determined by its [[virulence factor]]s.<ref>{{Cite web |url=http://mesh.kib.ki.se/swemesh/show.swemeshtree.cfm?Mesh_No=G06.930&tool=karolinska |title=MeSH - Medical Subject Headings, Karolinska Institute, 13 April 2010 |access-date=13 April 2010 |archive-date=3 March 2016 |archive-url=https://web.archive.org/web/20160303190453/http://mesh.kib.ki.se/swemesh/show.swemeshtree.cfm?Mesh_No=G06.930&tool=karolinska |url-status=dead }}</ref><ref>{{cite web|last1=Biology Online|title=Virulence|url=https://www.biologyonline.com/dictionary/virulence|website=Biology Online|date=7 October 2019}}</ref> In the specific context of [[Gene-for-gene relationship|gene for gene]] systems, often in plants, virulence refers to a pathogen's ability to infect a resistant host.<ref>{{Cite journal|last1=Thrall|first1=Peter H.|last2=Burdon|first2=Jeremy J.|year=2003|title=Evolution of Virulence in a Plant Host-Pathogen Metapopulation|journal=Science|language=en|volume=299|issue=5613|pages=1735–7|doi=10.1126/science.1080070|issn=0036-8075|pmid=12637745|bibcode=2003Sci...299.1735T|s2cid=6894315}}</ref> Virulence can also be transferred using a [[plasmid]]. The [[noun]] ''virulence'' ([[Latin]] noun {{lang|la|virulentia}}) derives from the [[adjective]] ''virulent'', meaning disease severity.<ref name="oxford">{{OED|virulent|id=223857}}</ref> The word ''virulent'' derives from the Latin word ''virulentus'', meaning "a poisoned wound" or "full of poison".<ref name="oxford" /><ref>{{Cite book|title=A Latin Dictionary |first1=Charlton T. |last1=Lewis |first2=Charles |last2=Short |chapter-url=http://www.perseus.tufts.edu/hopper/text?doc=Perseus%3Atext%3A1999.04.0059%3Aentry%3D%2351111 |chapter=vīrŭlentus |title-link=A Latin Dictionary |access-date=2023-01-02}}</ref> The term ''virulence'' does not only apply to viruses. From an [[ecology|ecological]] standpoint, virulence is the loss of [[fitness (biology)|fitness]] induced by a parasite upon its host. Virulence can be understood in terms of [[Proximate and ultimate causation|proximate causes]]—those specific traits of the pathogen that help make the host ill—and [[Proximate and ultimate causation|ultimate causes]]—the evolutionary pressures that lead to virulent traits occurring in a pathogen strain.<ref>{{Cite web|title=Plant disease | Importance, Types, Transmission, & Control | Britannica|url=https://www.britannica.com/science/plant-disease|access-date=2023-01-02|website=www.britannica.com|language=en}}</ref> ==Virulent bacteria== 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 factor]]s. Many virulence factors are so-called [[Bacterial effector protein|effector proteins]] that are injected into the host cells by specialized secretion apparati, such as the [[type three 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 (e.g., [[cytokine storm]]).{{cn|date=January 2025}} The virulence factors of bacteria are typically proteins or other molecules that are synthesized by [[enzyme]]s. These proteins are coded for by genes in [[chromosome|chromosomal]] DNA, [[bacteriophage]] DNA or [[plasmid]]s. 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.<ref>{{Cite journal | last1 = Keen | first1 = E. C. | title = Paradigms of pathogenesis: Targeting the mobile genetic elements of disease | doi = 10.3389/fcimb.2012.00161|journal=Frontiers in Cellular and Infection Microbiology|volume=2|page=161|year=2012|pmid = 23248780| pmc = 3522046| doi-access = free }}</ref> Bacteria use [[quorum sensing]] to synchronise release of the molecules. These are all proximate causes of morbidity in the host.{{cn|date=January 2025}} ===Methods by which bacteria cause disease=== ; Adhesion: Many bacteria must first bind to host cell surfaces. Many bacterial and host molecules that are involved in the adhesion of bacteria to host cells have been identified. Often, the host [[cell surface receptor]]s for bacteria are essential proteins for other functions. Due to the presence of [[mucus]] lining and of anti-microbial substances around some host cells, it is difficult for certain pathogens to establish direct contact-adhesion.{{cn|date=January 2025}} ; Colonization: Some virulent bacteria produce special proteins that allow them to colonize parts of the host body. ''[[Helicobacter pylori]]'' is able to survive in the acidic environment of the human stomach by producing the enzyme [[urease]]. Colonization of the stomach lining by this bacterium can lead to [[Peptic ulcer disease|gastric ulcers]] and [[Stomach cancer|cancer]]. The virulence of various strains of ''Helicobacter pylori'' tends to correlate with the level of production of urease.{{cn|date=January 2025}} ; Invasion: Some virulent bacteria produce proteins that either disrupt host cell membranes or stimulate their own [[endocytosis]] or [[Pinocytosis#Macropinocytosis|macropinocytosis]] into host cells. These virulence factors allow the bacteria to enter host cells and facilitate entry into the body across epithelial tissue layers at the body surface.{{cn|date=January 2025}} ; Immune response inhibitors: Many bacteria produce virulence factors that inhibit the host's immune system defenses. For example, a common bacterial strategy is to produce proteins that bind host antibodies. The [[polysaccharide]] [[Bacterial capsule|capsule]] of ''[[Streptococcus pneumoniae]]'' inhibits [[phagocytosis]] of the bacterium by host immune cells.{{cn|date=January 2025}} ; Toxins: Many virulence factors are proteins made by bacteria that poison host cells and cause tissue damage. For example, there are many [[Foodborne illness|food poisoning]] [[toxin]]s produced by bacteria that can contaminate human foods. Some of these can remain in "spoiled" food even after cooking and cause illness when the contaminated food is consumed. Other bacterial toxins are chemically altered and inactivated by the heat of cooking.{{cn|date=January 2025}} ==Virulent viruses== [[Virus]] virulence factors allow it to replicate, modify host defenses, and spread within the host, and they are toxic to the host.<ref name=Flint2009pp42-47>{{cite book|last1=Flint|first1=S.Jane|last2=Enquist|first2=Lynn W.|last3=Racaniello|first3=Vincent R.|last4=Skalka|first4=Anna Marie|title=Principles of Virology. Vol. II Pathogenesis and Control|year=2009|publisher=ASM|location=Washington, D.C.|isbn=978-1-55581-480-9|pages=42–7|edition=3rd}}</ref> 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 [[Endocytosis|endocytosed]] and the bound virus then enters the host cell. Virulent viruses such as [[HIV]], which causes [[HIV/AIDS|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]]. Many viruses can exist inside a host for long periods during which little damage is done. Extremely virulent strains can eventually [[Evolution|evolve]] by mutation and [[natural selection]] within the virus population inside a host. The term "[[Neurotropic virus|neurovirulent]]" is used for viruses such as [[rabies]] and [[herpes simplex]] which can invade the [[nervous system]] and cause disease there.{{cn|date=January 2025}} Extensively studied [[model organism]]s of virulent viruses include [[T4 phage|virus T4]] and other [[T-even bacteriophages]] which infect [[Escherichia coli]] and a number of related [[bacteria]].{{cn|date=January 2025}} The [[Lytic cycle|lytic life cycle]] of virulent bacteriophages is contrasted by the [[Lysogenic cycle|temperate lifecycle]] of temperate bacteriophages.<ref name=Brock>{{cite book | last1 = Madigan |first1=M. T. |last2=Martinko |first2=J. M. | title = Brock Biology of Microorganisms | edition=11th | publisher = Prentice Hall | year = 2006 | isbn = 978-0-13-144329-7 }}</ref><ref>{{Cite web|title=lytic phage | virus | Britannica|url=https://www.britannica.com/science/lytic-phage|access-date=2023-01-02|website=www.britannica.com|language=en}}</ref><!--Retrieved May 25, 2009, from Encyclopædia Britannica Online--> ==See also== {{col div|colwidth=30em}} * [[Host–pathogen interaction]] * [[Membrane vesicle trafficking]] * [[Bacterial effector protein]] * [[Infectious disease]] * {{annotated link|Law of declining virulence}} * [[Optimal virulence]] * [[Super-spreader]] * {{annotated link|Theory of virulence}} * [[Verotoxin-producing Escherichia coli]] * [[Virulence factor]] * [[Antivirulence]] {{colend}} ==References== {{commons category}} {{reflist}} {{Medical research studies}} [[Category:Microbiology terms]]
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