Rate of resistance evolution and polymorphism in long- and short-lived hosts

• Published in: Evolution Vol. 69; no. 2; pp. 551 - 560
• Main Authors: Bruns, Emily, Hood, Michael E., Antonovics, Janis
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01.02.2015; Society for the Study of Evolution; Oxford University Press
• Subjects: Animals; Anther smut; Basidiomycota; Biological Evolution; Biological resistance; BRIEF COMMUNICATIONS; Caryophyllaceae - microbiology; Density; Disease models; Disease resistance; Disease Resistance - genetics; Disease transmission; Epidemiology; Equilibrium; Evolution; generation time; Host-Pathogen Interactions; Life Cycle Stages; Longevity; Models, Genetic; Mortality; Parasite hosts; Pathogens; Plant Diseases - microbiology; Polymorphism; Polymorphism, Genetic; Qualitative research; resistance; sterilizing disease; Anther smut; longevity; sterilizing disease; polymorphism; generation time; resistance
• ISSN: 0014-3820; 1558-5646
• DOI: 10.1111/evo.12577

Recent theoretical work has shown that long-lived hosts are expected to evolve higher equilibrium levels of disease resistance than shorter-lived hosts, but questions of how longevity affects the rate of resistance evolution and the maintenance of polymorphism remain unanswered. Conventional wisdom suggests that adaptive evolution should occur more slowly in long-lived organisms than in short-lived organisms. However, the opposite may be true for the evolution of disease-resistance traits where exposure to disease, and therefore the strength of selection for resistance increases with longevity. In a single locus model of innate resistance to a frequency-dependent, sterilizing disease, longer lived hosts evolved resistance more rapidly than short-lived hosts. Moreover, resistance in long-lived hosts could only be polymorphic for more costly and more extreme resistance levels than short-lived hosts. The increased rate of evolution occurred in spite of longer generation times because longer-lived hosts had both a longer period of exposure to disease as well as higher disease prevalence. Qualitatively similar results were found when the model was extended to mortality-inducing diseases, or to density-dependent transmission modes. Our study shows that the evolutionary dynamics of host resistance is determined by more than just levels of resistance and cost, but is highly sensitive to the life-history traits of the host.