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比较恶性疟原虫对人类和黑猩猩基因组的作用:在三种黑猩猩亚种中,HBB 和 G6PD 上不存在疟疾基因组特征的证据。

The action of falciparum malaria on the human and chimpanzee genomes compared: absence of evidence for a genomic signature of malaria at HBB and G6PD in three subspecies of chimpanzee.

机构信息

Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK.

出版信息

Infect Genet Evol. 2009 Dec;9(6):1248-52. doi: 10.1016/j.meegid.2009.06.025. Epub 2009 Jul 22.

Abstract

The historical association between Plasmodium and primates has meant that many Plasmodium species have coevolved with specific primate hosts. However, unlike humans that are infected by species such as P. falciparum that cause severe malaria, many non-human primates are infected by Plasmodium species that only cause mild disease. Here we investigate whether the genomic signatures of plasmodial infection found in humans are also present in chimpanzees. We find no evidence of the major deleterious mutations at HBB (beta-globin) and G6PD in chimpanzees that confer resistance to malaria caused by P. falciparum nor evidence of long-term balancing selection at these loci. Our knowledge of malaria prevalence and pathogenesis in wild chimpanzees is severely limited, but it may be the case that beta-globin and G6PD variation are not adaptive in chimpanzees because malaria is rare and/or less detrimental in this species. Alternatively, chimpanzees may utilise mechanisms that are different from those of humans to protect against malaria.

摘要

疟原虫与灵长类动物之间的历史关联意味着许多疟原虫物种已经与特定的灵长类宿主共同进化。然而,与感染疟原虫 falciparum 等引起严重疟疾的人类不同,许多非人类灵长类动物感染的疟原虫只会引起轻微疾病。在这里,我们研究了在人类中发现的疟原虫感染的基因组特征是否也存在于黑猩猩中。我们没有发现黑猩猩中 HBB(β-珠蛋白)和 G6PD 上导致对疟原虫 falciparum 引起的疟疾产生抗性的主要有害突变的证据,也没有这些基因座上长期平衡选择的证据。我们对野生黑猩猩中疟疾的流行和发病机制的了解非常有限,但β-珠蛋白和 G6PD 变异在黑猩猩中可能不是适应性的,因为疟疾在这种物种中比较罕见和/或危害性较小。或者,黑猩猩可能利用与人类不同的机制来预防疟疾。

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