MHC influences infection with parasites and winter survival in the root vole Microtus oeconomus

Abstract

Selective pressure from parasites is thought to maintain the polymorphism of major histocompatibility complex (MHC) genes. Although a number of studies have shown a relationship between the MHC and parasitic infections, the fitness consequences of such associations are less well documented. In the present paper, we characterised the variation in exon 2 of MHC class II DRB gene in the root vole and examined the effects of that gene on parasite prevalence and winter survival. We identified 18 unique exon 2 sequences, which translated into 10 unique amino acid sequences. Phylogenetic analysis revealed the presence of three distinct clusters, and allele distributions among these individuals suggested that the clusters correspond to three different loci. Although the rate of synonymous substitutions (d S ) exceeded the rate of nonsynonymous substitutions (d N ) across sequences, implying purifying selection, d N was significantly elevated at antigen-binding sites, suggesting that these sites could be under positive selection. Screening for parasites revealed a moderate prevalence of infection with gastrointestinal parasites (24 % infected), but a high infection rate for blood parasites (56 % infected). Infection with the blood parasite Babesia ssp. decreased survival almost twofold (25.7 vs. 13.9 %). Animals possessing the amino acid sequence AA*08 survived better than others (44.9 vs. 22 %), and they were infected with Babesia ssp. less often (13.9 vs 25.7 %). In contrast, individuals carrying allele AA*05 were infected more often (31.7 vs. 15.3 %). Heterozygosity at one of the putative loci was associated with a lower probability of infection with Babesia ssp., but at the other locus, the association was reversed. The unexpected latter result could be at least partly explained by the increased frequency of the susceptible allele AA*05 among heterozygotes. Overall, we demonstrate that infection with Babesia ssp. is a strong predictor of Electronic supplementary material The online version of this article

Balancing selection and genetic drift at major histocompatibility complex class II genes in isolated populations of golden snub-nosed monkey (Rhinopithecus roxellana)

“…The putative ABS and non-ABS locations were derived according to the structure of human MHC II [85]. Compare with the method that used HLA-DR1 [86] structure to derive ABS sites, Reche and Reinherz’s research provided a better way to avoid the emergence of uncertain gaps while blasting DQ1 genes with DR1 genes, and was also adopted by other studies [87,88]. Historical selection evidence was obtained with Codeml in the Paml 4 package [89].…”

Adult survival selection in relation to multilocus heterozygosity and body size in a tropical bird species, the Zenaida dove, Zenaida aurita

“…Regarding the influence of genetic quality, both genomewide heterozygosity and heterozygosity at specific loci have been associated with increased survival in some vertebrate species (Schmeller et al 2007;Banks et al 2010;Evans et al 2010;Schaschl et al 2012;Kloch et al 2013;Forcada and Hoffman 2014), including birds (Redfield 1974;Markert et al 2004;Worley et al 2010;Sepil et al 2013). However, evidence for a direct effect of genomewide heterozygosity on survival remains limited, possibly because of methodological issues.…”

Parasite-mediated selection drives an immunogenetic trade-off in plains zebras (Equus quagga)

“…Further complications arise in disentangling the relative importance of different mechanisms due to antagonistic pleiotropic effects of multiple parasites on a single locus, such that resistance to different pathogens requires different MHC alleles or genotypes. Under pleiotropy, increased resistance to one pathogen may be accompanied by a cost through decreased resistance to another, resulting in perplexing associations between MHC alleles and increased susceptibility to infection [17,19,21,25,28,29]. Given that diverse parasites may act in concert or opposition to mediate selection on host MHC genes, incorporating knowledge about multiple parasite infections may lead to conclusions that would have otherwise gone undetected.…”