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Andrew F. Read, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK,
Sylvain Gandon, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK,
Sean Nee, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK,
Margaret J. Mackinnon, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT, UK
Pathogen evolution poses the critical challenge for infectious disease management in the twenty-first century. As is already painfully obvious in many parts of the world, the spread of drug-resistant and vaccine-escape (epitope) mutants can impair and even debilitate public and animal health programs. But there may also be another way in which pathogen evolution can erode the effectiveness of medical and veterinary interventions. Virulence- and transmission-related traits are intimately linked to pathogen fitness and are almost always genetically variable in pathogen populations. They can therefore evolve. Moreover, virulence and infectiousness are the target of medical and veterinary interventions. Here, we focus on vaccination and ask whether large-scale immunization programs might impose selection that results in the evolution of more-virulent pathogens.
The word virulence is used in a variety of ways in different disciplines. We take a parasite-centric view as follows. We use “disease severity” (morbidity and/or mortality) to mean the harm to the host following infection. Disease severity is thus a phenotype measured at the whole-organism (host) level that is determined by host genes, parasite genes, environmental effects, and the interaction between those factors. One component of this is virulence, a phenotypic trait of the pathogen whose expression depends on the host. Thus, virulence is the component of disease severity that is due to pathogen genes, and it can be measured only on a given host. We assume no specificity in the interaction between host and pathogen (more-virulent strains are always more virulent, whatever host they infect).
Many parasites exploit their host in order to accomplish within-host reproduction and allow transmission to new hosts. However, an extreme exploitation strategy may incur a cost since it might decrease the life expectancy of the host and, as a consequence, the chances of the parasite being transmitted. In this respect, virulence (i.e., the deleterious effect induced by the parasite) can be considered a byproduct of the parasite's host-exploitation strategy. Such a trade-off leads to the conclusion that parasites should evolve toward intermediate levels of virulence. This idea has been formalized by several authors (Anderson and May 1979; Ewald 1983; Van Baalen and Sabelis 1995a; Frank 1996c), who found that an evolutionarily stable level of virulence depends on several life-history parameters for both the host and parasite, as well as some constraints (such as the classic trade-off between transmission ability and virulence).
Moreover, it has been shown that multiple infections (i.e., the ability of the parasite to infect an already infected host) increase within-host competition and select for higher levels of virulence (Eshel 1977; Bremermann and Pickering 1983; Frank 1992a, 1994b, 1996c; Nowak and May 1994; May and Nowak 1995; Van Baalen and Sabelis 1995a). Several models have been developed around this idea (see Box 5.1), but we believe the kin-selection model proposed by Frank remains the simplest way to address this question (but see Box 11.1). Frank formalized the idea that there is a strong analogy between the evolution of altruism and that of parasite virulence.
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