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量化疾病抗性:更好地理解寄生虫对主要组织相容性复合体的介导选择。

Quantitative disease resistance: to better understand parasite-mediated selection on major histocompatibility complex.

机构信息

Department of Biology, Molecular Ecology and Evolution Lab, Lund University, Ecology Building, 223 62 Lund, Sweden.

出版信息

Proc Biol Sci. 2012 Feb 7;279(1728):577-84. doi: 10.1098/rspb.2011.0917. Epub 2011 Jul 6.

DOI:10.1098/rspb.2011.0917
PMID:21733902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3234550/
Abstract

We outline a descriptive framework of how candidate alleles of the immune system associate with infectious diseases in natural populations of animals. Three kinds of alleles can be separated when both prevalence of infection and infection intensity are measured--qualitative disease resistance, quantitative disease resistance and susceptibility alleles. Our descriptive framework demonstrates why alleles for quantitative resistance and susceptibility cannot be separated based on prevalence data alone, but are distinguishable on infection intensity. We then present a case study to evaluate a previous finding of a positive association between prevalence of a severe avian malaria infection (GRW2, Plasmodium ashfordi) and a major histocompatibility complex (MHC) class I allele (B4b) in great reed warblers Acrocephalus arundinaceus. Using the same dataset, we find that individuals with allele B4b have lower GRW2 infection intensities than individuals without this allele. Therefore, allele B4b provides quantitative resistance rather than increasing susceptibility to infection. This implies that birds carrying B4b can mount an immune response that suppresses the acute-phase GRW2 infection, while birds without this allele cannot and may die. We argue that it is important to determine whether MHC alleles related to infections are advantageous (quantitative and qualitative resistance) or disadvantageous (susceptibility) to obtain a more complete picture of pathogen-mediated balancing selection.

摘要

我们概述了一个描述性框架,说明免疫系统的候选等位基因如何与动物自然群体中的传染病相关联。当同时测量感染的流行率和感染强度时,可以分离出三种等位基因——定性疾病抗性、定量疾病抗性和易感性等位基因。我们的描述性框架表明,为什么仅基于流行率数据不能分离出定量抗性和易感性等位基因,但可以根据感染强度来区分。然后,我们提出了一个案例研究,以评估先前发现的一种严重禽疟感染(GRW2,Plasmodium ashfordi)与大苇莺 Acrocephalus arundinaceus 主要组织相容性复合体(MHC)I 类等位基因(B4b)之间存在正相关的发现。使用相同的数据集,我们发现携带等位基因 B4b 的个体的 GRW2 感染强度低于没有该等位基因的个体。因此,等位基因 B4b 提供定量抗性而不是增加感染易感性。这意味着携带 B4b 的鸟类可以产生抑制急性 GRW2 感染的免疫反应,而没有这种等位基因的鸟类则不能,并且可能死亡。我们认为,确定与感染相关的 MHC 等位基因是否对病原体介导的平衡选择有利(定量和定性抗性)或不利(易感性),对于获得更完整的病原体介导的平衡选择图景非常重要。

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