Study of pathogen evolution, particularly in the context of a host population that is undergoing changes in its density and structure, is crucial from the perspective of (i) understanding epidemiology of disease that is caused by pathogen emerging in a novel host, and (ii) understanding the effect of changing host population structure on major infectious diseases. We present an agent-based model that integrates mechanistic description of the within-host dynamics, between-host transmission, and the host population structure. In this framework, different strains of pathogens compete to (i) invade a host population, and (ii) persist by avoiding stochastic extinction at the host population level. We study the evolutionary dynamics of pathogen, in particular, its infection characterized by acuteness and the length of infection, when the between-host transmission and population structure are subject to change.

Results/Conclusions

We primarily focus on avirulent pathogens that result in life long immunity once the pathogen is cleared. When transmission is assumed to be proportionally dependent on the within-host pathogen density, and the host population to be homogeneously mixing, acute pathogens tend to have higher reproductive fitness and hence better at invading less acute pathogens. But they also tend to face higher risk of stochastic extinction at the host population level. This triggers an arms race in pathogen to progressively evolve higher acuteness until it pushes itself towards the brink of its own extinction. This self-destructive evolutionary dynamics is avoided when the between-host transmission relationship is assumed to be saturating with the within-host pathogen load, providing an evolutionarily stable pathogen characteristics. Similarly, population structure also plays an important role in mediating the pathogen evolution. When host population is structured into smaller interconnected patches, pathogens face an additional competition to invade population patches, favoring less acute and more persistent ones. As a result, pathogens with intermediate acuteness is selected.