Evolution of Pathogenicity and Virulence

Abstract

Evolutionary biologists define virulence as reduction in host fitness (survival and reproduction) caused by pathogens. The avirulence hypothesis posits that only recent host–pathogen interactions experience high virulence and pathogens inevitably evolve lower virulence over time. This hypothesis is now widely discredited because of weak empirical support and its erroneous dependence of group selection. Alternative models based on individual selection have replaced this view. The virulence-transmission tradeoff model is based on optimization of the pathogen’s within-host fitness (growth and reproduction) and between-host fitness (transmission). This model assumes that rapid pathogen reproduction (high within-host fitness) is associated with high virulence; however, high virulence may reduce between-host fitness, hence the need to optimize the tradeoff between the two. Two additional alternative models are the short-sighted evolution model and the coincidental evolution model. Coevolution involves reciprocal selection and adaptive genetic changes between interacting species. It frequently occurs in host–microbe interactions because the fitness of pathogen genotypes depends on host genotypes, and vice versa. The Red Queen model predicts dynamic polymorphisms with resistance alleles in hosts and infectivity alleles in pathogens cycling between high and low frequencies. This model also proposes that pathogens select for sex to generate genotypic diversity for adapting to changing host and pathogen genotypes.