期刊
NATURE MEDICINE
卷 9, 期 1, 页码 87-92出版社
NATURE AMERICA INC
DOI: 10.1038/nm807
关键词
-
资金
- NIAID NIH HHS [AI36478-07, AI46919-01A2, K23 AI049390, AI49390-01, R01 AI036478, R01 AI046919] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI036478, K23AI049390, R01AI046919, R01AI036478] Funding Source: NIH RePORTER
Geographic overlap between malaria and the occurrence of mutant hemoglobin and erythrocyte surface proteins has indicated that polymorphisms in human genes have been selected by severe malaria(1,2). Deletion of exon 3 in the glycophorin C gene (called GYPCDeltaex3 here) has been found in Melanesians; this alteration changes the serologic phenotype of the Gerbich (Ge) blood group system, resulting in Ge negativity(3,4). The GYPCDeltaex3 allele reaches a high frequency (46.5%) in coastal areas of Papua New Guinea where malaria is hyperendemic(5). The Plasmodium falciparum erythrocyte-binding antigen 140 (EBA140, also known as BAEBL)(6-8) binds with high affinity to the surface of human erythrocytes. Here we show that the receptor for EBA140 is glycophorin C (GYPC) and that this interaction mediates a principal P. falciparum invasion pathway into human erythrocytes. EBA140 does not bind to GYPC in Ge-negative erythrocytes, nor can P. falciparum invade such cells using this invasion pathway. This provides compelling evidence that Ge negativity has arisen in Melanesian populations through natural selection by severe malaria.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据