The role of host population heterogeneity in the evolution of virulence

Abstract

I examine here the effects of host heterogeneity in the growth of immune response on the evolution and co-evolution of virulence. The analysis is based on an extension of the 'nested model' by Gilchrist and Sasaki [Modeling host-parasite coevolution, J. Theor. Biol. 218 (2002), pp. 289-308]; the criteria for host and parasite evolution, in the paradigm of adaptive dynamics, for that model are derived in generality. Host heterogeneity is assumed to be fixed at birth according to a lognormal distribution or to the presence of two discrete types. In both cases, it is found that host heterogeneity determines a dramatic decrease in pathogen virulence, since pathogens will tune to the 'weakest' hosts. Finally we clarify how contrasting results present in the literature are due to different modelling assumptions.

On the principle of host evolution in host–pathogen interactions

“…We further find that if the pathogen increases its reproduction rate r, the optimal immune response rate of the host a * also increases. This is in agreement with prior results where a different principle for host evolution was used [26]. Finally, we use adaptive dynamics techniques to argue that the minimization of the case fatality proportion is an ESS for the host.…”

“…Figure 2 also suggests that as r increases, the optimal immune response rate a * also increases to compensate for the increased pathogen reproduction. This observation seems robust and was also made in the case when host lifespan in the infected class was considered as host optimization principle [17,26].…”

“…However, some forms of the mortality rate coupled with the form of β(τ ) may result in monotone CFP. Gilchrist and Sasaki [17] and Pugliese [26] assume the transmission rate β(τ ) proportional to the pathogen load. Comparison to data [22], however, suggests that the transmission rate is not linearly dependent on the pathogen load.…”

“…The case fatality proportion governs the outcome of the competition in both chronic diseases and diseases leading to recovery. Pugliese [26] suggested a different measure that governs the outcome of host competition, the lifespan in the infected class, but this measure is valid only if γ j (τ ) = 0, that is, recovery is impossible. Stability of E 1 will give the criterion for the outcome of host competition.…”

“…They used the lifespan of the host in the infectious class as a criterion for host evolution, assuming no natural mortality. Pugliese [26] later showed analytically that, even in the presence of natural mortality, the host evolves towards maximizing its lifespan in the infectious class. This measure, however, is not adequate for immuno-epidemiological models that model diseases with recovery.…”