Parasites may express proteins that mimic host proteins such that the host immune system cannot discriminate between host and parasite. An immune response to host proteins results in autoimmunity, and therefore, mechanisms to avert autoimmunity also limit the capacity of the immune system to respond to parasites that are mimics. In failing to elicit an immune response, parasites that are mimics appear to have a selective advantage and so it is unclear why all parasites do not evolve to be mimics. In this thesis, I demonstrate that next-generation methods can be used to perform an evolutionary invasion analysis. Subsequently, I use this method to identify evolutionarily stable strategies and to investigate three hypotheses for why all parasites are not mimics. These are: (1) that mimicry increases the risk of inducing autoimmunity and that hosts with autoimmunity are less likely to transmit the parasite; (2) that proteins which mimic host proteins have a reduced ability to perform the vital functions necessary for parasite replication; and (3) that owing to a feedback between the types of parasites that infect a host and the host's immune response, when parasites are likely to re-infect the same hosts, mimics are more likely to elicit an immune response. I show that each of these hypotheses explain why all parasites are not mimics. The key data needed to assess the applicability of these results is to quantify the number of secondary infections generated by hosts infected with parasites that are molecular mimics. This thesis motivates a new question in evolutionary epidemiology, furthers the field of evolutionary medicine and contributes novel methodologies for host-parasite multi-scale modelling in mathematical biology. / Thesis (Ph.D, Mathematics & Statistics) -- Queen's University, 2011-04-05 10:27:20.49