英美的研究人员说，非洲裔黑人身上特有的抗疟疾基因增加了他们感染艾滋病的机会。
据英国广播公司7月17日报道，非洲裔的黑人基因当中带有一种特有的抗疟疾基因。但是现在研究人员认为，这种基因妨碍了人体对抗早期艾滋病感染的能力。这次研究的主要目的是了解为何艾滋病会在非洲南部地区造成这么大的灾难。非洲至少有两千五百万人是艾滋病病毒携带者。
科学家在7月17日的《细胞—宿主与微生物》（Cell Host & Microbe）上发表的报告说，他们研究了一种叫做达菲的蛋白质，这种蛋白质能够阻止艾滋病病毒进入红血球。
但是九成的非洲裔黑人红血球表面没有这种蛋白质，也就是说这使得非洲裔黑人比较容易感染艾滋病。
令科学家感到奇怪的是，达菲蛋白质基因消退和非洲裔黑人特有的抗疟疾基因的演进过程似乎是同时并进的。
科学家是以美国黑人为研究对象，经过了25年的时间之后，做出此判断的。另外，虽然抗疟疾基因干扰达菲蛋白质，但是带有抗疟疾基因的艾滋病患者在发病之后，平均生命要比没有抗疟疾基因的患者长大约两年。
原始出处：
Cell Host & Microbe，Vol 4, 52-62, 17 July 2008，Weijing He, Sunil K. Ahuja
Duffy Antigen Receptor for Chemokines Mediates trans-Infection of HIV-1 from Red Blood Cells to Target Cells and Affects HIV-AIDS Susceptibility
Weijing He,1,2,9 Stuart Neil,3,9 Hemant Kulkarni,1,2,9 Edward Wright,3,9 Brian K. Agan,4,5,6,7 Vincent C. Marconi,4,5,7 Matthew J. Dolan,4,5,6,7,
Robin A. Weiss,3, and Sunil K. Ahuja1,2,8,
1 Veterans Administration Research Center for AIDS and HIV-1 Infection, South Texas Veterans Health Care System, San Antonio, TX 78229, USA
2 Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229, USA
3 Division of Infection and Immunity, University College London, London, UK
4 Infectious Disease Clinical Research Program, Uniformed Services University, Bethesda, MD 20814, USA
5 Infectious Disease Service, Wilford Hall United States Air Force Medical Center, Lackland Air Force Base, TX 78236, USA
6 Henry M. Jackson Foundation, Wilford Hall United States Air Force Medical Center, Lackland Air Force Base, TX 78236, USA
7 San Antonio Military Medical Center, Fort Sam Houston, TX 78234, USA
8 Department of Microbiology and Immunology, and Biochemistry, University of Texas Health Science Center, San Antonio, TX 78229, USA
Summary
Duffy antigen receptor for chemokines (DARC) expressed on red blood cells (RBCs) influences plasma levels of HIV-1-suppressive and proinflammatory chemokines such as CCL5/RANTES. DARC is also the RBC receptor for Plasmodium vivax. Africans with DARC −46C/C genotype, which confers a DARC-negative phenotype, are resistant to vivax malaria. Here, we show that HIV-1 attaches to RBCs via DARC, effecting trans-infection of target cells. In African Americans, DARC −46C/C is associated with 40% increase in the odds of acquiring HIV-1. If extrapolated to Africans, ∼11% of the HIV-1 burden in Africa may be linked to this genotype. After infection occurs, however, DARC-negative RBC status is associated with slower disease progression. Furthermore, the disease-accelerating effect of a previously described CCL5 polymorphism is evident only in DARC-expressing and not in DARC-negative HIV-infected individuals. Thus, DARC influences HIV/AIDS susceptibility by mediating trans-infection of HIV-1 and by affecting both chemokine-HIV interactions and chemokine-driven inflammation.
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