Optimal virulence
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Optimal virulence is a concept relating to the
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
Other
Evolutionary hypotheses
There are three main hypotheses about why a pathogen evolves as it does. These three models help to explain the
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
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
See also
- Law of declining virulence– Disproved hypothesis of epidemiologist Theobald Smith
References
- ^ 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. - ^ 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.
- PMID 15306410.
- PMID 15355551.
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