Article ID Journal Published Year Pages File Type
4499897 Mathematical Biosciences 2015 14 Pages PDF
Abstract

•Within- and between-host pathogen dynamics are modeled, linked by pathogen shedding.•With no host co-infection, the clone with the highest R0 eliminates all others.•With host co-infection, low shedding rates are favored within co-infected hosts.•Mortality, transmission rates and within-host dynamics affect competition outcome.•Trade-offs between within- and between-host effects can allow clone coexistence.

A model linking within- and between-host pathogen dynamics via pathogen shedding (emission of pathogens throughout the course of infection) is developed, and several aspects of host availability and co-infection are considered. In this model, the rate of pathogen shedding affects both the pathogen population size within a host (also affecting host mortality) and the rate of infection of new hosts. Our goal is to ascertain how the rate of shedding is likely to evolve, and what factors permit coexistence of alternative shedding rates in a pathogen population. For a constant host population size (where an increase in infected hosts necessarily decreases susceptible hosts), important differences arise depending on whether pathogens compete only for susceptible (uninfected) hosts, or whether co-infection allows for competition for infected hosts. With no co-infection, the pathogen type that can persist with the lowest number of susceptible hosts will outcompete any other, which under the assumptions of the model is the pathogen with the highest basic reproduction number. This is often a pathogen with a relatively high shedding rate (s). If within-host competition is allowed, a trade-off develops due to the conflicting effects of shedding on within- and between-host pathogen dynamics, with within-host competition favoring clones with low shedding rates while between-host competition benefits clones with higher shedding rates. With within-host competition for the same host cells, low shedding rate clones should eliminate high-s clones in a co-infected host, if equilibrium is reached. With co-infection, but no within-host competition, pathogen clones still interact by affecting the mortality of co-infected hosts; here, coexistence is more likely. With co-infection, two clones can coexist if one is the superior competitor for uninfected hosts and the other for co-infected hosts.

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