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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N-glycolylneuraminic acid
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Evolution of human-chimpanzee differences in malaria susceptibility: Relationship to human genetic loss of N-glycolylneuraminic acid

机译：人类-黑猩猩对疟疾易感性差异的演变：与人类遗传性N-羟乙酰神经氨酸损失的关系

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摘要

Chimpanzees are the closest evolutionary cousins of humans, sharing > 99% identity in most protein sequences. Plasmodium falciparum is the major worldwide cause of malaria mortality. Plasmodium reichenowi, a morphologically identical and genetically very similar parasite, infects chimpanzees but not humans. Conversely, experimental P. falciparum infection causes brief moderate parasitization and no severe infection in chimpanzees. This surprising host specificity remains unexplained. We modified and enhanced traditional methods for measuring sialic acid (Sia)dependent recognition of glycophorins by merozoite erythrocyte-binding proteins, eliminating interference caused by endogenous Sias on transfected cells, and by using erythroleukemia cells to allow experimental manipulation of Sia content. We present evidence that these remarkable differences among such closely related host-parasite pairs is caused by species-specific erythrocyte-recognition profiles, apparently related to the human-specific loss of the common primate Sia N-glycolylneuraminic acid. The major merozoite-binding protein erythrocyte-binding antigen-175 of P. falciparum apparently evolved to take selective advantage of the excess of the Sia N-acetylneuraminic acid (the precursor of N-glycolyineuraminic acid) on human erythrocytes. The contrasting preference of P. reichenowi erythrocyte-binding antigen-175 for N-glycolyineuraminic acid is likely the ancestral condition. The surprising ability of P. falciparum to cause disease in New World Aotus monkeys (geographically isolated from P. falciparum until arrival of peoples from the Old World) can be explained by parallel evolution of a human-like Sia expression pattern in these distantly related primates. These results also have implications for the prehistory of hominids and for the genetic origins and recent emergence of P. falciparum as a major human pathogen.
机译：黑猩猩是人类最接近的进化表亲，在大多数蛋白质序列中具有> 99％的同一性。恶性疟原虫是全世界疟疾死亡的主要原因。瑞氏疟原虫是一种形态完全相同且遗传上非常相似的寄生虫，它会感染黑猩猩，但不会感染人类。相反，实验性恶性疟原虫感染会引起短暂的中度寄生，而黑猩猩则不会出现严重感染。这种令人惊讶的宿主特异性仍然无法解释。我们修改和增强了传统方法，该方法通过裂殖子红细胞结合蛋白测量唾液酸（Sia）依赖性糖蛋白的识别，消除内源性Sias对转染细胞的干扰，并使用红白血病细胞进行Sia含量的实验操作。我们提供的证据表明，在这些密切相关的宿主-寄生虫对之间的这些显着差异是由物种特异性的红细胞识别谱引起的，显然与普通灵长类动物Sia N-羟乙酰神经氨酸的人特异性丧失有关。恶性疟原虫的主要裂殖子结合蛋白红细胞结合抗原-175显然进化为利用人类红细胞上过量的Sia N-乙酰神经氨酸（N-糖基尿酸的前体）。 Reichenowi红细胞结合抗原175对N-糖基尿酸尿酸的对比偏爱很可能是祖先的情况。在这些远缘的灵长类动物中类似人的Sia表达模式的平行进化可以解释恶性疟原虫在新大陆Aotus猴子中致病的惊人能力（在地理上与恶性疟原虫隔离，直到旧世界的人们到达）。 。这些结果也对原始人的史前史，恶性疟原虫作为主要人类病原体的遗传起源和最近出现产生了影响。

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