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Virulence
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Virulence (also called pestiferousness) refers to the degree of pathogenicity of an organism, or in other words the relative ability of a pathogen to cause disease.
The word virulent, which is the adjective for virulence, derives from the Latin word virulentus, which means "full of poison." From an ecological point of view, virulence can be defined as the host's parasite-induced loss of fitness.
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.
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Encyclopedia
Virulence (also called pestiferousness) refers to the degree of pathogenicity of an organism, or in other words the relative ability of a pathogen to cause disease.
The word virulent, which is the adjective for virulence, derives from the Latin word virulentus, which means "full of poison." From an ecological point of view, virulence can be defined as the host's parasite-induced loss of fitness.
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 factors. 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 protein enzymes. These proteins are coded for by genes in chromosomal DNA, bacteriophage DNA or plasmids.
Methods by which pathogens 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 receptors for bacteria are essential proteins for other functions.
- 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 Gastric ulcer and cancer. The virulence of various strains of Helicobacter pylori tends to corellate with the level of production of urease.
- Invasion. Some virulent bacteria produce proteins that either disrupt host cell membranes or stimulate endocytosis 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.
- 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 capsule of Streptococcus pneumoniae inhibits phagocytosis of the bacterium by host immune cells.
- Toxins. Many virulence factors are proteins made by bacteria that poison host cells and cause tissue damage. For example, there are many food poisoning toxins 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. Some bacterial toxins are chemically altered and inactivated by the heat of cooking.
Virulent virus
Viral virulence factors 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 the AIDS virus. 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 .
Evolution of Virulence
The pathogen population will evolve once in the host. There are three main beliefs on how and why the pathogen evolves. These three models help to explain why viruses or bacteria reproduce or migrate within the host and may even kill the host. The three hypotheses are the Coincidental Evolution Hypothesis, Short-Sighted Evolution Hypothesis, and Trade-Off Hypothesis.
Short Sighted Evolution Hypothesis
The theory behind short-sighted evolution is that the traits that increase Darwinian fitness will rise to high frequency within the population. These traits include abilities to live longer, reproduce in higher numbers, survive against antibodies, or survive in other areas of the body that the pathogen does not normally infiltrate. These traits typically arise due to mutations, which are seen in greater numbers in pathogens than in hosts. After only a few generations the beneficial mutations will rise to high frequency. Although the mutations may increase the fitness of the pathogen, they can be detrimental to the host causing much harm. It would seem to be that the pathogen would stop reproducing or increasing in number once the population reached the point of harming the host, because the host is the supply of nutrients for the bacteria or virus. But since the natural selection of mutations is not an intelligently controlled process, the pathogens do not stop growing or reproducing, even when the host is being damaged to the point of death.
Coincidental Evolution Hypothesis
The mechanisms that naturally transforming bacteria have for picking up free DNA from the environment, protecting it from destruction by restriction enzymes, and incorporating it into their genomes are complex and highly evolved. A number of hypotheses have been presented for the selective pressures responsible for the evolution of transformation. One of these is consistent with a coincidental evolution hypothesis. The virulence of many pathogens in humans may not be a target of selection itself, but rather an accidental by-product of selection on other traits. An example of this is a soil bacterium called Clostridium tetani, which causes tetanus. Tetanus, when entering a human wound, can grow and divide rapidly. While dividing, tetanus produces a neurotoxin that makes tetanus highly infectious and highly lethal. Humans can not transfer this bacteria and tetanus do not live in humans initially. Its not the selection inside humans that give the bacterium to produce this toxin, but rather the selection of its normal life cycle within the soil.
Trade-off Hypothesis
Biologists first believed that pathogenic populations would evolve to ever decreasing virulence because damage to the host will ultimately be harmful to the pathogen living inside. For example, if the host dies, the pathogen will die too. Therefore, it was believed that less virulent pathogens should have more life-time reproductive success. This is not entirely the case. Pathogens that accelerate the death of their host can rise in frequency if the pathogen adequately increases its chances of being transmitted. Therefore, there should be a balance between the costs and benefits of virulence during the evolution of pathogens.
See also
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