Virulence is a pathogen's or microorganism's ability to cause damage to a host.
In most, especially in animal systems, virulence refers to the degree of damage caused by a microbe to its host.[1] The pathogenicity of an organism—its ability to cause disease—is determined by its virulence factors.[2] [3] In the specific context of gene for gene systems, often in plants, virulence refers to a pathogen's ability to infect a resistant host.[4]
The noun virulence (Latin noun Latin: virulentia) derives from the adjective virulent, meaning disease severity. The word virulent derives from the Latin word virulentus, meaning "a poisoned wound" or "full of poison."[5] The term virulence does not only apply to viruses.
From an ecological standpoint, virulence is the loss of fitness induced by a parasite upon its host. Virulence can be understood in terms of proximate causes—those specific traits of the pathogen that help make the host ill—and ultimate causes—the evolutionary pressures that lead to virulent traits occurring in a pathogen strain.[6]
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 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).
The virulence factors of bacteria are typically proteins or other molecules that are synthesized by enzymes. 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.[7] Bacteria use quorum sensing to synchronise release of the molecules. These are all proximate causes of morbidity in the host.
Virus virulence factors allow it to replicate, modify host defenses, and spread within the host, and they are toxic to the host.[8]
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. 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. Many viruses can exist inside a host for long periods during which little damage is done. Extremely virulent strains can eventually evolve by mutation and natural selection within the virus population inside a host. The term "neurovirulent" is used for viruses such as rabies and herpes simplex which can invade the nervous system and cause disease there.
Extensively studied model organisms of virulent viruses include virus T4 and other T-even bacteriophages which infect Escherichia coli and a number of related bacteria.
The lytic life cycle of virulent bacteriophages is contrasted by the temperate lifecycle of temperate bacteriophages.[9] [10]