As early as Haldane (1949) , and as more recently underscored (Frank, 2002; Lazzaro and Little, 2009) , it has been recognized that parasites drive polymorphisms in host immune competence, particularly in variable environments. This can occur by balancing (Wegner, 2008) or disruptive selection (Duffy et al., 2008; Matthews et al., 2010) . High levels of polymorphism are found in several genes of both the innate and adaptive immune systems (Hill, 2001; Trowsdale and Parham, 2004; Acevedo-Whitehouse and Cunningham, 2006) . MHC genes show a predominance of non-synonymous over synonymous mutations in their peptidebinding regions, and have extensive allelic diversity, indicative of strong role of selection, generally considered to be mediated by parasites. For example, parasite pressure is believed to have promoted maintenance of high MHC diversity in sticklebacks (Wegner et al., 2003) and Atlantic salmon (Dionne et al., 2007) . In humans, regional differences in HLA class I diversity has been associated with intracellular parasite richness (Prugnolle et al., 2005) . Across species comparisons of rodents have associated helminth species richness with increased MHC class II polymorphisms (de Bellocq et al., 2008) . MHC genes are also known for their role in mediating mate choice through olfactory systems in humans (McClintock et al., 2002) , rodents (Sommer, 2005) , and fishes (Landry et al., 2001; Milinski et al., 2005) .