ECOLOGICAL PERSPECTIVES ON HOST-PARASITE COEVOLUTION

It is a truth universally acknowledged that polymorphism at host immunity loci and corresponding parasite antigenicity loci, maintained by coevolution in pathosystems, is common and can persist for millions of years. Such polymorphisms and how they persist or break down are both fundamentally interesting and important for human health and agriculture. Examples include the major histocompatibility complex in vertebrates and the gene-for-gene (GFG) relationships in plants and their parasites. GFG systems are well-understood genetically and an important source of disease resistance for plant breeders. Therefore considerable effort has gone into studying their evolutionary dynamics in natural pathosystems and modelling the conditions under which long-term polymorphism persists or breaks down. Polymorphism in GFG systems is common and in many cases ancient in wild pathosystems. Conversely, in agriculture the introduction of a resistance gene normally results in the matching parasite avirulence gene rapidly becoming locally extinct. Simple genetic models of GFG coevolution do not produce stable polymorphism. Various more complex models do but are difficult to analyse. Recent work has shown a factor common to stable models is negative direct frequency-dependent selection, so at least one genotype becomes less fit as it grows more common regardless of genotype frequencies in the other species. This selection is not present in simplified models, but is generated in real pathosystems by various ecological and epidemiological factors. Here I expand on previous work by demonstrating that realistic demography, specifically density-dependent regulation of parasite incidence, can generate negatively self-regulating stabilising pressure. This is loosely analogous to negative frequency-dependent selection and, similarly, can stabilise polymorphism in GFG pathosystems. I show this density-dependent regulation can stabilise both non-spatial deterministic and spatial stochastic systems. I also study how this stabilising factor interacts with the complicating biological factors of limited dispersal and resultant spatial structure in populations, variable host density and the presence of a second parasite.

Name dc:type.qualificationname

phd

Level dc:type.qualificationlevel

doctoral

Grantor dc:publisher.institution

University of East Anglia

Year dc:date.issued

2013

Author dc:creator

• Dobbie, Samuel Thormond

Language dc:language

en