Sin Yung Wa, Annavi Geetha, Dugdale Hannah L, Newman Chris, Burke Terry, MacDonald David W
Wildlife Conservation Research Unit, Department of Zoology, Recanati-Kaplan Centre, University of Oxford, Tubney House, Abingdon Road, Tubney, Abingdon, Oxfordshire, OX13 5QL, UK; NERC Biomolecular Analysis Facility, Department of Animal and Plant Sciences, University of Sheffield, Sheffield, S10 2TN, UK; Department of Organismic and Evolutionary Biology, Museum of Comparative Zoology, Harvard University, 26 Oxford Street, Cambridge, MA, 02138, USA.
Mol Ecol. 2014 Oct;23(20):5072-88. doi: 10.1111/mec.12917. Epub 2014 Oct 7.
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.
病原体介导的选择被认为通过杂合子优势、稀有等位基因优势和波动选择机制维持主要组织相容性复合体（MHC）基因的极端多样性。当同时考虑多种病原体时，杂合子优势（即比纯合子识别和结合更广泛的抗原范围）预计更易被检测到。在此，我们测试欧洲獾（Meles meles）野生种群中的MHC多样性是否由病原体介导的选择驱动。我们检查了来自一系列分类群的13种病原体的个体患病率（是否感染）、感染强度和共感染情况，并研究了它们与MHC I类和II类变异性的关系。该种群的MHC等位基因数量可变但相对较少，且受到多种自然存在的病原体感染，这使其非常适合用于研究MHC与病原体的关系。我们发现病原体感染与特定的MHC单倍型和等位基因之间存在关联。共感染状态与MHC杂合性无关，但有证据表明杂合子对个体病原体感染具有优势。这表明稀有等位基因优势和/或波动选择以及杂合子优势可能是塑造该物种MHC多样性的选择力量。我们发现MHC与感染强度之间的关联证据比与患病率之间的更强，并得出结论，同时检查病原体患病率和感染强度很重要。此外，检查大量且多样的病原体以及MHC I类和II类基因（它们具有不同功能），能更好地理解驱动MHC多样性的机制。
