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Chapter Two - Genetic diversity and disease spread: epidemiological models and empirical studies of a snail–trematode system

from Part I - Understanding within-host processes

Published online by Cambridge University Press:  28 October 2019

Kenneth Wilson
Affiliation:
Lancaster University
Andy Fenton
Affiliation:
University of Liverpool
Dan Tompkins
Affiliation:
Predator Free 2050 Ltd
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Summary

For simplicity’s sake, standard population genetic models of host–parasite coevolution often exclude ecological and epidemiological detail. In particular, they assume that each host is exposed to a single infectious propagule, regardless of the parasite’s prevalence. On the other hand, standard epidemiological models usually assume that all hosts are equally susceptible to infection. Here, we summarise models in which we relax these simplifying assumptions, thereby allowing for feedbacks between evolution, ecology, and epidemiology. One major result from these models is that, under certain general conditions, a parasite’s potential for disease spread (R0) decreases as genetic diversity for resistance increases in the host population. Moreover, R0 can increase if we allow the parasite population to track common host genotypes. Feedbacks between ecology and evolution mean that as a common genotype comes to dominate the host population, the parasite population adapts to preferentially infect this genotype, increasing the prevalence of infection and the mean number of parasite exposures per host. We further connect these findings to the major evolutionary hypothesis that coevolving parasites can favour sexual reproduction.

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Chapter
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Wildlife Disease Ecology
Linking Theory to Data and Application
, pp. 32 - 57
Publisher: Cambridge University Press
Print publication year: 2019

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References

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