Elevated viral recombination in short-lived hosts

Recombination (including reassortment) is a salient force in viral evolution and has been implicated in the emergence of several zoonotic pathogens in humans. Viral recombination occurs during simultaneous infection of an individual host with multiple genotypes (co-infection). Thus, processes which affect the incidence of a disease in the host population affect how often viral genotypes recombine. We investigate whether and how host traits affect the realized rate of viral recombination using a mathematical model that makes feedbacks between viral evolution and host ecology (in particular, lifespan) explicit. Our main result is that viruses of host species that are short-lived tend to recombine more frequently than those of relatively long-lived hosts. This is because of differences in population density and, thus, the prevalence of (co-)infection at equilibrium. Using highly pathogenic avian influenza sequence data, we test the prediction that recombination is elevated in short-lived hosts. In agreement with this prediction, the magnitude of statistical associations between mutations on different segments of the flu genome increases with host body size, a proxy for lifespan. Similarly, estimates of the reassortment rate from phylogenetic network analyses decrease with body size. We discuss the implications of these findings for disease emergence. Subject categoryEvolution Subject areasevolution, health and disease and epidemiology, ecology