Meeting Abstract
Variation in host competence can lead some individuals to contribute disproportionately to pathogen transmission. Exposure to anthropogenic stressors that impair immune performance could increase the proportion of “supershedding” individuals and thus alter the size and duration of epidemics. In order to predict how living in stressful environments influences outbreak severity requires models that couple stress-mediated immune function in individuals to population-level transmission dynamics. Here I use a within-host model of immune cell-pathogen interactions to investigate how stressors that restrict the energy allocated to immune defense determine pathogen colonization and host infectious period. At the population level I assume that individuals vary in their acquisition and allocation of resources in stressful environments, and use the within-host model to generate a distribution of infectious periods. Finally I couple within and between host processes by simulating epidemics on this heterogeneous host population. This approach represents an initial attempt to incorporate natural and stress-induced variation into infection models that bridge immunological and epidemiological scales.
