Optimal virulence

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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 offspring to other hosts. For about 100 years, the consensus was that virulence decreased and parasitic relationships evolved toward symbiosis. This was even called the law of declining virulence despite being a hypothesis, not even a theory. It has been challenged since the 1980s and has been disproved. [1] [2]

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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.

Mode of transmission

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 field hospitals and trench warfare provided an easy route to transmission that evolved the virulence of the 1918 influenza pandemic. In such immobilized, crowded conditions pathogens can make individuals very sick and still jump to healthy individuals.

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 virulence 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, studies of the malaria parasite using rodent [3] and chicken [4] models 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 do 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. The optimum conditions for high virulence would be a community with immune dysfunction (and/or poor hygiene and sanitation) that was in all other ways as healthy as possible (eg optimum nutrition).

See also

Related Research Articles

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Parasitism is a close relationship between species, where one organism, the parasite, lives on or inside another organism, the host, causing it some harm, and is adapted structurally to this way of life. The entomologist E. O. Wilson characterised parasites as "predators that eat prey in units of less than one". Parasites include single-celled protozoans such as the agents of malaria, sleeping sickness, and amoebic dysentery; animals such as hookworms, lice, mosquitoes, and vampire bats; fungi such as honey fungus and the agents of ringworm; and plants such as mistletoe, dodder, and the broomrapes.

Virulence is a pathogen's or microorganism's ability to cause damage to a host.

Viral evolution is a subfield of evolutionary biology and virology that is specifically concerned with the evolution of viruses. Viruses have short generation times, and many—in particular RNA viruses—have relatively high mutation rates. Although most viral mutations confer no benefit and often even prove deleterious to viruses, the rapid rate of viral mutation combined with natural selection allows viruses to quickly adapt to changes in their host environment. In addition, because viruses typically produce many copies in an infected host, mutated genes can be passed on to many offspring quickly. Although the chance of mutations and evolution can change depending on the type of virus, viruses overall have high chances for mutations.

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<span class="mw-page-title-main">Evolution of sexual reproduction</span> How sexually reproducing multicellular organisms could have evolved from a common ancestor species

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<span class="mw-page-title-main">Unit of selection</span> Biological entity within the hierarchy of biological organization

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<i>Francisella tularensis</i> Species of bacterium

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<span class="mw-page-title-main">Vertically transmitted infection</span> Infection caused by pathogens that use mother-to-children transmission

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<span class="mw-page-title-main">Lysogenic cycle</span> Process of virus reproduction

Lysogeny, or the lysogenic cycle, is one of two cycles of viral reproduction. Lysogeny is characterized by integration of the bacteriophage nucleic acid into the host bacterium's genome or formation of a circular replicon in the bacterial cytoplasm. In this condition the bacterium continues to live and reproduce normally, while the bacteriophage lies in a dormant state in the host cell. The genetic material of the bacteriophage, called a prophage, can be transmitted to daughter cells at each subsequent cell division, and later events can release it, causing proliferation of new phages via the lytic cycle.

Any cause that reduces or increases reproductive success in a portion of a population potentially exerts evolutionary pressure, selective pressure or selection pressure, driving natural selection. It is a quantitative description of the amount of change occurring in processes investigated by evolutionary biology, but the formal concept is often extended to other areas of research.

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<span class="mw-page-title-main">Avian malaria</span> Parasitic disease of birds

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<i>Evolution of Infectious Disease</i>

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When considering pathogens, host adaptation can have varying descriptions. For example, in the case of Salmonella, host adaptation is used to describe the "ability of a pathogen to circulate and cause disease in a particular host population." Another usage of host adaptation, still considering the case of Salmonella, refers to the evolution of a pathogen such that it can infect, cause disease, and circulate in another host species.

<span class="mw-page-title-main">Andrew F. Read</span>

Andrew Fraser Read FRS is Evan Pugh professor of biology and entomology at Pennsylvania State University and the Director of the Huck Institutes of the Life Sciences.

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References

  1. Fall, Ed; Yates, Christian (1 February 2021). "Will coronavirus really evolve to become less deadly?". The Conversation . Retrieved 29 November 2021. The trade-off model is now widely accepted. It emphasises that each host-pathogen combination must be considered individually. There is no general evolutionary law for predicting how these relationships will pan out, and certainly no justification for evoking the inevitability of decreased virulence.
    There is little or no direct evidence that virulence decreases over time. While newly emerged pathogens, such as HIV and Mers, are often highly virulent, the converse is not true. There are plenty of ancient diseases, such as tuberculosis and gonorrhoea, that are probably just as virulent today as they ever were.
  2. Orent, Wendy (16 November 2020). "Will the Coronavirus Evolve to Be Less Deadly? - History and science suggesting many possible pathways for pandemics, but questions remain about how this one will end". Smithsonian Magazine . Retrieved 29 November 2020.
  3. Mackinnon, M; A Read (2004). "Virulence in malaria: an evolutionary viewpoint". Philosophical Transactions of the Royal Society B . 359 (1446): 965–986. doi:10.1098/rstb.2003.1414. PMC   1693375 . PMID   15306410.
  4. 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: 30. doi: 10.1186/1471-2148-4-30 . PMC   520815 . PMID   15355551.