Abstract

A key feature of the vertebrate adaptive immune system is acquired immune memory, whereby hosts launch a faster and heightened response when challenged by previously encountered pathogens, preventing full infection. Here, we use a mathematical model to explore the role of ecological and epidemiological processes in shaping selection for costly acquired immune memory. Applying the framework of adaptive dynamics to the classic SIR (Susceptible-Infected-Recovered) epidemiological model, we focus on the conditions that may lead hosts to evolve high levels of immunity. Linking our work to previous theory, we show how investment in immune memory may be greatest at long or intermediate host lifespans depending on whether immunity is long lasting. High initial costs to gain immunity are also found to be essential for a highly effective immune memory. We also find that high disease infectivity and sterility, but intermediate virulence and immune period, increase selection for immunity. Diversity in host populations through evolutionary branching is found to be possible but only for a limited range of parameter space. Our model suggests that specific ecological and epidemiological conditions have to be met for acquired immune memory to evolve.

Highlights

  • An adaptive immune system appears to exist in almost all vertebrates (Cooper and Alder 2006)

  • Ecology and Evolution published by John Wiley & Sons Ltd

  • An acquired immune memory formed by memory T- and B-cells is common across vertebrate populations and there is widespread interest in how this immune response has evolved (Cooper and Alder 2006; Litman et al 2010; Hirano et al 2011)

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Summary

Introduction

An adaptive immune system appears to exist in almost all vertebrates (Cooper and Alder 2006). There are still important insights to be gained for our understanding of how the ecological and epidemiological environment of hosts and parasites may have initially shaped selection for immune memory, of the apparent discrepancy in investment in immunity with host lifespan (Miller et al 2007) and of the fundamental differences between populations with (SIRtype models) and without (Susceptible-Infected-Susceptible [SIS]-type models) immune memory.

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