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      MHC-I provides both quantitative resistance and susceptibility to blood parasites in blue tits in the wild

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      Journal of Avian Biology
      Wiley-Blackwell

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            Enhanced immunological surveillance in mice heterozygous at the H-2 gene complex.

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              Pathogen resistance and genetic variation at MHC loci.

              Balancing selection in the form of heterozygote advantage, frequency-dependent selection, or selection that varies in time and/or space, has been proposed to explain the high variation at major histocompatibility complex (MHC) genes. Here the effect of variation of the presence and absence of pathogens over time on genetic variation at multiallelic loci is examined. In the basic model, resistance to each pathogen is conferred by a given allele, and this allele is assumed to be dominant. Given that s is the selective disadvantage for homozygotes (and heterozygotes) without the resistance allele and the proportion of generations, which a pathogen is present, is e, fitnesses for homozygotes become (1 - s)((n - 1)e) and the fitnesses for heterozygotes become (1 - s)((n - 2)e), where n is the number of alleles. In this situation, the conditions for a stable, multiallelic polymorphism are met even though there is no intrinsic heterozygote advantage. The distribution of allele frequencies and consequently heterozygosity are a function of the autocorrelation of the presence of the pathogen in subsequent generations. When there is a positive autocorrelation over generations, the observed heterozygosity is reduced. In addition, the effects of lower levels of selection and dominance and the influence of genetic drift were examined. These effects were compared to the observed heterozygosity for two MHC genes in several South American Indian samples. Overall, resistance conferred by specific alleles to temporally variable pathogens may contribute to the observed polymorphism at MHC genes and other similar host defense loci.
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                Journal
                Journal of Avian Biology
                J Avian Biol
                Wiley-Blackwell
                09088857
                September 2016
                September 2016
                : 47
                : 5
                : 669-677
                Article
                10.1111/jav.00830
                05ce3314-f0dc-49d2-aa1e-3448f26348c8
                © 2016

                http://doi.wiley.com/10.1002/tdm_license_1.1

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