Tue . 19 Jun 2019

Optimal virulence

optimal virulence factors, optimal virulence meaning
Optimal virulence is a concept relating to the ecology of hosts and parasites One definition of virulence is the host's parasite-induced loss of fitness The parasite's fitness is determined by its success in transmitting offsprings to other hosts At one time, the consensus was that over time, virulence moderated and parasitic relationships evolved toward symbiosis This view has been challenged A pathogen that is too restrained will lose out in competition to a more aggressive strain that diverts more host resources to its own reproduction However, the host, being the parasite's resource and habitat in a way, suffers from this higher virulence This might induce faster host death, and act against the parasite's fitness by reducing probability to encounter another host killing the host too fast to allow for transmission Thus, there is a natural force providing pressure on the parasite to "self-limit" virulence The idea is, then, that there exists an equilibrium point of virulence, where parasite's fitness is highest Any movement on the virulence axis, towards higher or lower virulence, will result in lower fitness for the parasite, and thus will be selected against

Contents

  • 1 Mode of transmission
  • 2 Evolutionary hypotheses
    • 21 Trade-off hypothesis
    • 22 Short-sighted evolution hypothesis
    • 23 Coincidental evolution hypothesis
  • 3 Expansion into new environments
  • 4 Host susceptibility
  • 5 References
  • 6 External links

Mode of transmission

According to evolutionary medicine, virulence increases with horizontal transmission between non-relatives and decreases with vertical transmission from parent to child

Paul W Ewald has explored the relationship between virulence and mode of transmission He came to the conclusion that virulence tends to remain especially high in waterborne and vector-borne infections, such as cholera and Dengue Cholera is spread through sewage and Dengue through mosquitos In the case of respiratory infections, the pathogen depends on an ambulatory host to survive It must spare the host long enough to find a new host Water- or vector-borne transmission circumvents the need for a mobile host Ewald is convinced that the crowding of trench warfare provided an easy route to transmission that explains the virulence of the 1918 influenza pandemic In crowded conditions the time to find a new host is minimal

Other epidemiologists have expanded on the idea of a tradeoff between costs and benefits of virulence One factor is the time or distance between potential hosts Airplane travel, crowded factory farms and urbanization have all been suggested as possible sources of virulence Another factor is the presence of multiple infections in a single host leading to increased competition among pathogens In this scenario, the host can survive only as long as it resists the most virulent strains The advantage of a low virulence strategy becomes moot Multiple infections can also result in gene swapping among pathogens, increasing the likelihood of lethal combinations

Evolutionary hypotheses

There are three main hypotheses about why a pathogen evolves as it does These three models help to explain the life history strategies of parasites, including reproduction, migration within the host, virulence, etc The three hypotheses are the Trade-Off Hypothesis, the Short-Sighted Evolution Hypothesis, and the Coincidental Evolution Hypothesis All of these offer ultimate explanations for virulence in pathogens

Trade-off hypothesis

At one time, some biologists argued that pathogens would tend to evolve toward ever decreasing virulence because the death of the host or even serious disability is ultimately harmful to the pathogen living inside For example, if the host dies, the pathogen population inside may die out entirely Therefore, it was believed that less virulent pathogens that allowed the host to move around and interact with other hosts should have greater success reproducing and dispersing

But this is not necessarily the case Pathogen strains that kill the host can increase in frequency as long as the pathogen can transmit itself to a new host, whether before or after the host dies The evolution of virulence in pathogens is a balance between the costs and benefits of virulence to the pathogen For example, Mackinnon and Read 2004 and Paul et al 2004 studied the malaria parasite using a rodent and chicken model respectively and found that there was trade-off between transmission success and virulence as defined by host mortality

Short-sighted evolution hypothesis

Short-sighted evolution suggests that the traits that increase reproduction rate and transmission to a new host will rise to high frequency within the pathogen population These traits include the ability to reproduce sooner, reproduce faster, reproduce in higher numbers, live longer, survive against antibodies, or survive in parts of the body the pathogen does not normally infiltrate These traits typically arise due to mutations, which occur more frequently in pathogen populations than in host populations, due to the pathogens' rapid generation time and immense numbers After only a few generations, the mutations that enhance rapid reproduction or dispersal will increase in frequency The same mutations that enhance the reproduction and dispersal of the pathogen also enhance its virulence in the host, causing much harm disease and death If the pathogen's virulence kills the host and interferes with its own transmission to a new host, virulence will be selected against But as long as transmission continues despite the virulence, virulent pathogens will have the advantage So, for example, virulence often increases within families, where transmission from one host to the next is likely, no matter how sick the host Similarly, in crowded conditions such as refugee camps, virulence tends to increase over time since new hosts cannot escape the likelihood of infection

Coincidental evolution hypothesis

Some forms of pathogenic virulence did not co-evolve with the host For example, tetanus is caused by the soil bacterium Clostridium tetani After C tetani bacteria enter a human wound, the bacteria may grow and divide rapidly, even though the human body is not their normal habitat While dividing, C tetani produce a neurotoxin that is lethal to humans But it is selection in the bacterium's normal life cycle in the soil that leads it to produce this toxin, not any evolution with a human host The bacterium finds itself inside a human instead of in the soil by mere happenstance We can say that the neurotoxin is not directed at the human host

More generally, the virulence of many pathogens in humans may not be a target of selection itself, but rather an accidental by-product of selection that operates on other traits, as is the case with antagonistic pleiotropy

Expansion into new environments

A potential for virulence exists whenever a pathogen invades a new environment, host or tissue The new host is likely to be poorly adapted to the intruder, either because it has not built up an immunological defense or because of a fortuitous vulnerability In times of change, natural selection favors mutations that exploit the new host more effectively than the founder strain, providing an opportunity for virulence to erupt

Host susceptibility

Host susceptibility contributes to virulence Once transmission occurs, the pathogen must establish an infection to continue The more competent the host immune system, the less chance there is for the parasite to survive It may require multiple transmission events to find a suitably vulnerable host During this time, the invader is dependent upon the survival of its current host For this reason virulence thrives in a community with prevalent immune dysfunction and poor nutrition Virulence weakens in a healthy population and as hosts acquire resistance Good hygiene, nutrition and sanitation are all effective strategies against virulence

References

  1. ^ Mackinnon, M; A Read 2004 "Virulence in malaria: an evolutionary viewpoint" Philosophical Transactions of the Royal Society B 359 1446 doi:101098/rstb20031414 
  2. ^ Paul, R; T Lafond; CDM Muller-Graf; S Nithiuthai; PT Brey; JC Koella 2004 "Experimental evaluation of the relationship between lethal or non-lethal virulence and transmission success in malaria parasite infections" BMC Evolutionary Biology 4 doi:101186/1471-2148-4-30 

External links

  • Empirical Support for Optimal Virulence in a Castrating Parasite
  • Evolution of Virulence
  • Adaptive Dynamics of Infectious Diseases: In Pursuit of Virulence
  • Integrating across levels Interesting discussion of the complexity of optimal virulence theory
  • `Small worlds' and the evolution of virulence: infection occurs
  • Pathogen Virulence: The Evolution of Sickness - A Review from the Science Creative Quarterly

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    Optimal virulence beatiful post thanks!

    29.10.2014


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