女科学家《Nature》改写HIV历史

　　

生物通报道，美国阿拉巴马大学伯明翰分校的Beatrice Hahn教授在最新一期的Nature上发表了HIV研究的最新进展，Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz，改写了HIV研究史。

 

艾滋病的起源一直是科学家们研究重点，获得最多人拥护的观点是，艾滋病病毒HIV来自于猩猩的SIV，猩猩通过血液将其传播给人类，SIV再突变进化成HIV（SIV为HIV的祖先），导致艾滋病在人群中大面积传播。一直引众多科学家困惑的是，猩猩感染SIV后并不发病，也没有艾滋病样的症状。所以，科学家们就认为猩猩对SIV具有天然免疫力。

 

然而，Beatrice Hahn教授在历经多年的研究获得的新观点将改写科学家这20年来对SIV的观点。究小组已经收集了足够的数据证实SIV对猩猩的影响，这些数据为重新审视SIV与猩猩的关系提供了一手证据。Beatrice Hahn教授曾在今年的16届逆转录病毒与机会性感染年会上发表这一观点，做了详细的专题报告

（具体见先前报道：http://www.ebiotrade.com/newsf/2009-2/2009213170640.htm）

 

在坦桑尼亚为期9年的研究中发现，冈贝国家公园内9%—18%的黑猩猩在研究期间感染了SIV。在成年黑猩猩中，感染SIV者死亡风险是未感染者的10—16倍，而感染SIV的婴儿黑猩猩全部死亡。

 

研究人员注意到，其中一只雌性黑猩猩在感染SIV后3年内死亡，并在之前表现出与人类艾滋病相似的虚弱和倦怠等症状。解剖后发现，其身体消瘦，被寄生虫感染完全破坏，免疫细胞严重衰竭，这些也与人类艾滋病相似。

 

研究小组之后比较了其它死亡黑猩猩（感染或未感染SIV）的组织标本，结果发现感染SIV者的CD4 T细胞水平反常地低，而CD4 T细胞正是HIV靶向和破坏的细胞类型。综合这些发现表明，SIV会对黑猩猩造成严重的、类似艾滋病的影响。

 

美国国立过敏与传染病研究所的Daniel Douek对这项研究大加赞赏，他说：“从进化和流行病学观点来看，这些数据可看作是HIV流行历史上‘缺失的一环’”。

 

此次研究表明，科学家将不可能在黑猩猩基因组内找到HIV免疫性的“钥匙”，不过它也为科学家打下了基础，通过研究不同灵长类动物对于HIV/SIV的反应，来获得HIV和SIV如何导致宿主患病的深入理解。

（生物通 小茜）

生物通推荐原文检索：

Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz

 

Brandon F. Keele1,17, James Holland Jones4, Karen A. Terio5, Jacob D. Estes6, Rebecca S. Rudicell2, Michael L. Wilson7,8, Yingying Li1, Gerald H. Learn1, T. Mark Beasley3, Joann Schumacher-Stankey8, Emily Wroblewski8, Anna Mosser9, Jane Raphael9, Shadrack Kamenya9, Elizabeth V. Lonsdorf10, Dominic A. Travis11, Titus Mlengeya12, Michael J. Kinsel5, James G. Else13, Guido Silvestri14, Jane Goodall15, Paul M. Sharp16, George M. Shaw1, Anne E. Pusey8 & Beatrice H. Hahn1,2

 

Department of Medicine,

Department of Microbiology,

Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA

Department of Anthropology, Stanford University, Stanford, California 94305, USA

University of Illinois Zoological Pathology Program, Maywood, Illinois 60153, USA

The AIDS and Cancer Virus Program, Science Applications International Corporation-Frederick Inc., National Cancer Institute-Frederick, Frederick, Maryland 21702, USA

Department of Anthropology, University of Minnesota, Minneapolis, Minnesota 55455, USA

Jane Goodall Institute's Center for Primate Studies, Department of Ecology, Evolution and Behavior, University of Minnesota, St Paul, Minnesota 55108, USA

Gombe Stream Research Centre, The Jane Goodall Institute, Kigoma, Tanzania

The Lester E. Fisher Center for the Study and Conservation of Apes and,

Department of Conservation and Science, Lincoln Park Zoo, Chicago, Illinois 60614, USA

Tanzania National Parks, Arusha, Tanzania

Division of Animal Resources, Yerkes National Primate Research Center, Emory University, Atlanta, Georgia 30322, USA

Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19107, USA

The Jane Goodall Institute, Arlington, Virginia 22203, USA

Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3JT, UK

Present address: The AIDS and Cancer Virus Program, Science Applications International Corporation-Frederick Inc., National Cancer Institute-Frederick, Frederick, Maryland 21702, USA.

 

【Abstract】

African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2)1, 2. Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts3. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4+ T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4+ T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.