In most pathogens, epidemiological and evolutionary processes occur on similar time scales due to large population sizes and short generation times. Thus, the interplay of ecology and evolution is particularly relevant and amenable to study in these systems, especially in the context of pathogen diversity. How diversity is maintained over time and how it influences epidemiological processes are active areas of research, of relevance to control. A component of 'fitness differences' is the ability of the pathogen to bind the host receptors. Heterogeneity in host receptor types in the population can allow coexistence of strains that evolve specialization for these different host 'resources'. Here, we ask how this evolutionary outcome is modified by consideration of frequency-dependent competition for hosts due to specific immunity (niche differences), and specifically, what is the outcome when changes in binding affinity are not independent from the degree of cross-immunity. Motivated by emerging evidence that rotavirus utilizes different human blood group antigens for cell entry, we implemented an adaptive dynamics framework to analyze the interplay of these two kinds of variation on the long-term stable coexistence of multiple strains in an extended SIR model.
Results/Conclusions
Our results indicate that a strong trade-off in host-pathogen affinity together with strong cross-immunity is required for long-term coexistence. Furthermore, the coexistence of semi-specialized pathogens is possible when cross-immunity is a function of host-pathogen affinity. In this case, numerical results show the coexistence of multiple non-specialized strains as the result of repeated evolutionary branching. These results denote the importance of considering both immunity and host heterogeneity in understanding the long-term coexistence of multiple pathogen strains and, in particular, how niche differentiation can be influenced by host affinity as well as immune response. This consideration is of relevance as changes in the receptor binding site can also modify the recognition by the immune system, with epidemiological consequences that are still poorly understood.