An ecological role for assortative mating under infection?

Wildlife diseases are emerging at a higher rate than ever before meaning that understanding their potential impacts is essential, especially for those species and populations that may already be of conservation concern. The link between population genetic structure and the resistance of populations to disease is well understood: high genetic diversity allows populations to better cope with environmental changes, including the outbreak of novel diseases. Perhaps following this common wisdom, numerous empirical and theoretical studies have investigated the link between disease and disassortative mating patterns, which can increase genetic diversity. Few however have looked at the possible link between disease and the establishment of assortative mating patterns. Given that assortative mating can reduce genetic variation within a population thus reducing the adaptive potential and long-term viability of populations, we suggest that this link deserves greater attention, particularly in those species already threatened by a lack of genetic diversity. Here, we summarise the potential broad scale genetic implications of assortative mating patterns and outline how infection by pathogens or parasites might bring them about. We include a review of the empirical literature pertaining to disease-induced assortative mating. We also suggest future directions and methodological improvements that could advance our understanding of how the link between disease and mating patterns influences genetic variation and long-term population viability.

Population genetic structure of serotine bats (Eptesicus serotinus) across Europe and implications for the potential spread of bat rabies (European bat lyssavirus EBLV-1).

Understanding of the movements of species at multiple scales is essential to appreciate patterns of population connectivity and in some cases, the potential for pathogen transmission. The serotine bat (Eptesicus serotinus) is a common and widely distributed species in Europe where it frequently harbours European bat lyssavirus type 1 (EBLV-1), a virus causing rabies and transmissible to humans. In the United Kingdom, it is rare, with a distribution restricted to south of the country and so far the virus has never been found there. We investigated the genetic structure and gene flow of E. serotinus across the England and continental Europe. Greater genetic structuring was found in England compared with continental Europe. Nuclear data suggest a single population on the continent, although further work with more intensive sampling is required to confirm this, while mitochondrial sequences indicate an east-west substructure. In contrast, three distinct populations were found in England using microsatellite markers, and mitochondrial diversity was very low. Evidence of nuclear admixture indicated strong male-mediated gene flow among populations. Differences in connectivity could contribute to the high viral prevalence on the continent in contrast with the United Kingdom. Although the English Channel was previously thought to restrict gene flow, our data indicate relatively frequent movement from the continent to England highlighting the potential for movement of EBLV-1 into the United Kingdom.