Within-host population dynamics and the evolution of microparasites in a heterogeneous host population

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Within-host population dynamics and the evolution of microparasites in a heterogeneous host population

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Title: Within-host population dynamics and the evolution of microparasites in a heterogeneous host population
Author: Ganusov, Vitaly V.; Bergstrom, Carl T.; Antia, Rustom
Abstract: Why do parasites harm their hosts? The general understanding is that if the transmission rate and virulence of a parasite are linked, then the parasite must harm its host in order to maximize its transmission. The exact nature of such trade-offs remains largely unclear, but for vertebrate hosts, it probably involves interactions between a microparasite and the host immune system. Previous results have suggested that in a homogeneous host population in the absence of super- or coinfection, within host dynamics lead to selection of the parasite with an intermediate growth rate which is just being controlled by the immune system before it kills the host (Antia et al. 1994). In this paper, we examine how this result changes when heterogeneity is introduced to the host population. We incorporate the simplest form of heterogeneity - random heterogeneity in the parameters describing the size of the initial parasite innoculum, the immune response of the host and the lethal density at which the parasite kills the host. We find that the general conclusion of the previous model holds: parasites evolve some intermediate growth rate. However in contrast with the generally accepted view we find virulence does not necessarily decrease with increasing heterogeneity. We find that the most appropriate measures of virulence, such as the case mortality rate of infected hosts or the population mortality rate, increase with heterogeneity. However if we use the innoculum size which proves lethal to fifty percent of infected hosts (LD-50) as a measure of virulence, then virulence initially decreases and then subsequently increases with increasing levels of heterogeneity. Finally, we link the within-host and between-host dynamics of pathogens: we show how the parameters for epidemiological spread of the disease can be estimated from the within-host dynamics, and in doing so examine the way in which trade-offs between these epidemiological parameters arise as a consequence of the interaction of the parasite and the immune response of the host.
URI: http://hdl.handle.net/1773/1997

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