Spatial extension of the theoretical framework of the adaptive virulence evolution hypothesis

The adaptive virulence hypothesis states that parasites cause death to their hosts because virulence is beneficial for the transmission and spread of parasites. A growing body of empirical evidence supports the adaptive virulence hypothesis but more examples are needed for its empirical validation. The classic mathematical framework of the adaptive virulence hypothesis does not account for host population structure which can have important implications for virulence evolution. The goal of this thesis is to address the broad applicability problems and extend spatially the mathematical framework of the adaptive virulence hypothesis by accounting for host movement in the model. My thesis examines whether virulence is adaptive at the species level by investigating the relationship between virulence and parasite fitness using simulation data. I find that virulence and parasite fitness, measured as the basic reproduction number R0, are correlated at the between-species level and the exact form of the relationship depends on the selective pressures within each group of parasite species. Also, I break free from the classic framework of the adaptive virulence hypothesis to investigate virulence evolution when parasites reduce host movement. The results explain the transient coexistence of low- and high-virulence strains in Avian influenza viruses. I reviewed epidemic models with host movement to understand what aspects of disease spread are important to develop a spatially extended model for virulence evolution. I find that epidemic models with spatially heterogeneous epidemiological parameters, like disease transmissibility, are suitable for the spatial extension of the mathematical framework of the adaptive virulence hypothesis. Finally, I investigated the relationship between the temporal and the spatial spread of infectious diseases. I show an inverse relationship between the initial epidemic growth rate and the spatial spread rate which may reflect a trade-off between parasites dispersal and transmission. Overall my thesis opens interesting research avenues for future works to formulate spatially explicit models for the evolution of virulence and makes significant contributions to the empirical investigation of the adaptive virulence hypothesis and the role of animal movement for disease spread and virulence evolution