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Pathogen burden,co‐infection and major histocompatibility complex variability in the European badger (Meles meles)
Authors:Yung Wa Sin  Geetha Annavi  Hannah L Dugdale  Chris Newman  Terry Burke  David W MacDonald
Institution:1. Wildlife Conservation Research Unit, Department of Zoology, Recanati‐Kaplan Centre, University of Oxford, , Tubney, Abingdon, Oxfordshire, OX13 5QL UK;2. NERC Biomolecular Analysis Facility, Department of Animal and Plant Sciences, University of Sheffield, , Sheffield, S10 2TN UK;3. Department of Organismic and Evolutionary Biology, Museum of Comparative Zoology, Harvard University, , Cambridge, MA, 02138 USA;4. Faculty of Science, Department of Biology, University of Putra Malaysia, , Serdang, Selangor, Malaysia;5. Behavioural Ecology and Self‐Organization, University of Groningen, , 9700 CC Groningen, the Netherlands;6. Theoretical Biology, University of Groningen, , 9700 CC Groningen, the Netherlands
Abstract:Pathogen‐mediated selection is thought to maintain the extreme diversity in the major histocompatibility complex (MHC) genes, operating through the heterozygote advantage, rare‐allele advantage and fluctuating selection mechanisms. Heterozygote advantage (i.e. recognizing and binding a wider range of antigens than homozygotes) is expected to be more detectable when multiple pathogens are considered simultaneously. Here, we test whether MHC diversity in a wild population of European badgers (Meles meles) is driven by pathogen‐mediated selection. We examined individual prevalence (infected or not), infection intensity and co‐infection of 13 pathogens from a range of taxa and examined their relationships with MHC class I and class II variability. This population has a variable, but relatively low, number of MHC alleles and is infected by a variety of naturally occurring pathogens, making it very suitable for the investigation of MHC–pathogen relationships. We found associations between pathogen infections and specific MHC haplotypes and alleles. Co‐infection status was not correlated with MHC heterozygosity, but there was evidence of heterozygote advantage against individual pathogen infections. This suggests that rare‐allele advantages and/or fluctuating selection, and heterozygote advantage are probably the selective forces shaping MHC diversity in this species. We show stronger evidence for MHC associations with infection intensity than for prevalence and conclude that examining both pathogen prevalence and infection intensity is important. Moreover, examination of a large number and diversity of pathogens, and both MHC class I and II genes (which have different functions), provide an improved understanding of the mechanisms driving MHC diversity.
Keywords:evolutionary arms race  frequency‐dependent selection  heterozygote advantage hypothesis  host–  parasite co‐evolution  pathogen‐mediated selection  rare‐allele advantage
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