摘要

Invertebrate immune priming, and other forms of innate immune memory in bacteria, plants, and mammals, modulate the post-infection resistance, tolerance, and survival phenotypes of individuals previously exposed to microbes. By influencing the probability of both transmission and disease-induced mortality, priming is likely to have a significant impact on disease dynamics. Two alternative models have been proposed as frameworks for the role of priming in infected populations, but the differences in their underlying key assumptions yield very different predictions for the effect of priming on disease dynamics. By examining these assumptions from the lens of within-host dynamics, the model presented in this paper demonstrates that priming systems can be characterized along a continuous dose-response gradient that unites these disparate frameworks. Moreover, it facilitates the incorporation of different kinds of immunological plasticity mechanisms, as well as the exposure probability and transmission characteristics of parasites. Simulating the interaction of these thresholds with the diversity of parasite life history strategies and distributions predicts that priming may actually inflate disease prevalence under certain conditions. Thus, priming of innate immune systems may act analogously to leaky vaccines and drive parasite virulence evolution. The results underscore the need for experimental studies that determine dose response curves for the both the probability of becoming primed following primary parasite exposure and shifts in resistance and tolerance in infected primed hosts. This framework is applicable to a variety of systems that show immunological memory.

  • 出版日期2017-3