A large body of literature on the ‘monoculture effect’ has shown that host genetic diversity can strongly affect infectious disease dynamics. Specifically, genetically diverse host populations can decrease the prevalence of infectious diseases. These ecological dynamics have been shown across plants and animals for decades and, recently, attention has also been turning to the evolutionary effects of host genetic diversity on infectious disease. Studies using mathematical theory and experimental evolution suggest that evolution along genetically identical hosts selects for more virulent pathogens. The mathematical theory suggests that this is because the pathogen is released from trade-offs between adapting to different host genotypes. Because the parasite does not have to adapt to infecting a second host genotype, it can become fully specialized and therefore more virulent on the focal host type. This is supported by a large body of literature on local adaptation that seems to suggest that pathogens are generally more capable of exploiting hosts from their local environment than from more distant ones.
For my dissertation, I plan to examine the evolutionary effects of host genetic diversity on viral evolution through a series of experimental evolution studies in our lab’s Plodia interpunctella and granulosis virus model system. Because the mathematical theory predicts that these evolutionary effects are due to trade-offs between adapting to different host genotypes, further work on this question in the system depends on the existence of these specific interactions. Furthermore, the plodia laboratory system is fairly unique in that we can alter the viscosity of the food medium to increase the spatial structuring or mixing of the larval population. This technique will allow me to expand upon the existing experimental evolution studies that measure virulence evolution on homogeneous or heterogeneous host types to also ask how the spatial mixing or structuring of the host genotypes affects parasite evolution. We may expect that the “distance” between host genotypes in an infection network would affect the importance of adapting to all genotypes in the population.
For my dissertation, I plan to examine the evolutionary effects of host genetic diversity on viral evolution through a series of experimental evolution studies in our lab’s Plodia interpunctella and granulosis virus model system. Because the mathematical theory predicts that these evolutionary effects are due to trade-offs between adapting to different host genotypes, further work on this question in the system depends on the existence of these specific interactions. Furthermore, the plodia laboratory system is fairly unique in that we can alter the viscosity of the food medium to increase the spatial structuring or mixing of the larval population. This technique will allow me to expand upon the existing experimental evolution studies that measure virulence evolution on homogeneous or heterogeneous host types to also ask how the spatial mixing or structuring of the host genotypes affects parasite evolution. We may expect that the “distance” between host genotypes in an infection network would affect the importance of adapting to all genotypes in the population.
