英美的研究人員說，非洲裔黑人身上特有的抗瘧疾基因增加了他們感染艾滋病的機(jī)會(huì),。
據(jù)英國廣播公司7月17日?qǐng)?bào)道,，非洲裔的黑人基因當(dāng)中帶有一種特有的抗瘧疾基因。但是現(xiàn)在研究人員認(rèn)為,，這種基因妨礙了人體對(duì)抗早期艾滋病感染的能力,。這次研究的主要目的是了解為何艾滋病會(huì)在非洲南部地區(qū)造成這么大的災(zāi)難。非洲至少有兩千五百萬人是艾滋病病毒攜帶者,。
科學(xué)家在7月17日的《細(xì)胞—宿主與微生物》（Cell Host & Microbe）上發(fā)表的報(bào)告說,，他們研究了一種叫做達(dá)菲的蛋白質(zhì)，這種蛋白質(zhì)能夠阻止艾滋病病毒進(jìn)入紅血球,。
但是九成的非洲裔黑人紅血球表面沒有這種蛋白質(zhì),，也就是說這使得非洲裔黑人比較容易感染艾滋病。
令科學(xué)家感到奇怪的是,，達(dá)菲蛋白質(zhì)基因消退和非洲裔黑人特有的抗瘧疾基因的演進(jìn)過程似乎是同時(shí)并進(jìn)的,。
科學(xué)家是以美國黑人為研究對(duì)象，經(jīng)過了25年的時(shí)間之后,，做出此判斷的,。另外，雖然抗瘧疾基因干擾達(dá)菲蛋白質(zhì),，但是帶有抗瘧疾基因的艾滋病患者在發(fā)病之后,，平均生命要比沒有抗瘧疾基因的患者長大約兩年。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
