Abstract
Current theory for the regulation of host populations by pathogens suggests that a high level of suppression during the initial epidemic phase will be followed by a population rebound with decreased virulence due to pathogen and host evolution, and the extent of host suppression increases with increasing pathogen transmissibility (R0) and virulence. Using simple epidemiological models, we explore the effect of three factors on short- and long-term suppression: the strength of density-dependent population regulation (homeostasis); maternal antibodies, and age-dependent mortality. Rapid homeostasis can mitigate long-term population suppression, and surprisingly weak homeostasis can even result in a greater population suppression during the endemic phase compared to the initial epidemic. Maternal antibodies can significantly reduce suppression of the host population if they attenuate rather than block infections. A similar result obtains if the severity of disease is lower in the young than in adults. In both cases, a higher R0 can result in lower suppression, and the average virulence can decline over time without any (genetic) evolution. Our results suggest the need for a nuanced view of long-term suppression by a new pathogen, with the outcome sensitive to many details even in the absence of evolution.