人类ABO多态性在两种互补选择压力下的进化。
Evolution of the human ABO polymorphism by two complementary selective pressures.
作者信息
Seymour Robert M, Allan Martin J, Pomiankowski Andrew, Gustafsson Kenth
机构信息
Department of Mathematics, University College London, Gower Street, London, UK.
出版信息
Proc Biol Sci. 2004 May 22;271(1543):1065-72. doi: 10.1098/rspb.2004.2674.
The best-known example of terminal-glycan variation is the ABO histo-blood group polymorphism in humans. We model two selective forces acting on histo-blood group antigens that may account for this polymorphism. The first is generated by the invasion of opportunistic bacterial or other pathogens that interact with the epithelial-mucosal surfaces. The bacteria adapt to the microenvironments of common host phenotypes and so create frequency-dependent selection for rarer host alleles. The second is generated by intracellular viruses, and accounts for the observed differentials between the ABO-phenotype frequencies. It is thought that viruses acquire histo-blood group structures as part of their envelope from their previous host. The presence of host antigens on the viral envelope causes differential transmission of the virus between host types owing to the asymmetric action of ABO natural antibodies. Our model simulations show that these two forces acting together can account for the major features of the ABO polymorphism in humans.
终末聚糖变异最著名的例子是人类的ABO组织血型多态性。我们建立了两种作用于组织血型抗原的选择力模型，这可能解释了这种多态性。第一种是由与上皮-粘膜表面相互作用的机会性细菌或其他病原体的入侵产生的。细菌适应常见宿主表型的微环境，因此对较罕见的宿主等位基因产生频率依赖性选择。第二种是由细胞内病毒产生的，解释了观察到的ABO表型频率差异。据认为，病毒从其先前宿主那里获得组织血型结构作为其包膜的一部分。病毒包膜上宿主抗原的存在，由于ABO天然抗体的不对称作用，导致病毒在不同宿主类型之间的传播差异。我们的模型模拟表明，这两种力共同作用可以解释人类ABO多态性的主要特征。
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