為了確定HIV是否正在適應(yīng) “人白細(xì)胞抗原”（HLA）等位基因,，如HLA-B*57,、B*57 和B*51等 （它們對HIV病毒的成功控制進(jìn)行調(diào)控），研究人員對來自北美,、加勒比,、歐洲、非洲,、大洋洲及太平洋諸島和亞洲的超過500位HIV感染者進(jìn)行了病毒序列及HLA類型分析,。
他們的結(jié)果顯示，為響應(yīng)免疫選擇壓力,，HIV正在人口層面上進(jìn)行演化,。雖然這并不表明HIV肯定會贏得與人類之間的這場演化爭斗,，但它的確說明，我們將需要成功的HIV疫苗（就像流感疫苗一樣）,，來與變化中的免疫環(huán)境保持同步,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 458, 641-645 (2 April 2009) | doi:10.1038/nature07746
Adaptation of HIV-1 to human leukocyte antigen class I
Yuka Kawashima1, Katja Pfafferott3,6, John Frater4,5, Philippa Matthews3, Rebecca Payne3, Marylyn Addo7, Hiroyuki Gatanaga2,8, Mamoru Fujiwara1, Atsuko Hachiya1,8, Hirokazu Koizumi1, Nozomi Kuse1, Shinichi Oka2,8, Anna Duda4,5, Andrew Prendergast3, Hayley Crawford3, Alasdair Leslie3, Zabrina Brumme7, Chanson Brumme7, Todd Allen7, Christian Brander7,9, Richard Kaslow10, James Tang10, Eric Hunter11, Susan Allen12, Joseph Mulenga12, Songee Branch13, Tim Roach13, Mina John6, Simon Mallal6, Anthony Ogwu14, Roger Shapiro14, Julia G. Prado3, Sarah Fidler15, Jonathan Weber15, Oliver G. Pybus16, Paul Klenerman4,5, Thumbi Ndung'u17, Rodney Phillips4,5, David Heckerman19, P. Richard Harrigan18, Bruce D. Walker7,17,20, Masafumi Takiguchi1 & Philip Goulder3,6,17
1 Divisions of Viral Immunology and,
2 Infectious Disease, Center for AIDS Research, Kumamoto University, 2-2-1 Honjo, Kumamoto 860-0811, Japan
3 Department of Paediatrics,
4 Nuffield Department of Clinical Medicine and,
5 The James Martin 21st Century School, Peter Medawar Building for Pathogen Research, South Parks Road, Oxford OX1 3SY, UK
6 Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital and Murdoch University, Western Australia 6000, Australia
7 Partners AIDS Research Center, Massachusetts General Hospital, 13th Street, Building 149, Charlestown, Boston, Massachusetts 02129, USA
8 AIDS Clinical Center, International Medical Center of Japan, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan
9 Fundació IrsiCaixa-HIVACAT, Hospital Germans Trias i Pujol, Badalona and Institucio Catalana de Recerca i Estudis Avancats (ICREA), Barcelona 08916, Spain
10 University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
11 Emory University Vaccine Center and Yerkes National Primate Research Center, Atlanta, Georgia 30329, USA
12 Zambia Emory HIV Research Project, and the Zambia Blood Transfusion Service, Lusaka, Zambia
13 Ladymeade Reference Unit, University of West Indies, Bridgetown BB11156, Barbados
14 Botswana-Harvard School of Public Health AIDS Initiative Partnership, Gaborone, Botswana
15 Division of Medicine, Wright Fleming Institute, Imperial College, St Mary's Hospital, Norfolk Place, Paddington, London W2 1PG, UK
16 Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3SY, UK
17 HIV Pathogenesis Programme, The Doris Duke Medical Research Institute, University of KwaZulu-Natal, Durban 4013, South Africa
18 Miscrosoft Research, One Microsoft Way, Redmond, Washington 9805, USA
19 BC Centre for Excellence in HIV/AIDS, Vancouver, British Columbia V6Z 1Y6, Canada
20 Howard Hughes Medical Institute, Chevy Chase, Maryland 20185, USA
The rapid and extensive spread of the human immunodeficiency virus (HIV) epidemic provides a rare opportunity to witness host–pathogen co-evolution involving humans. A focal point is the interaction between genes encoding human leukocyte antigen (HLA) and those encoding HIV proteins. HLA molecules present fragments (epitopes) of HIV proteins on the surface of infected cells to enable immune recognition and killing by CD8+ T cells; particular HLA molecules, such as HLA-B*57, HLA-B*27 and HLA-B*51, are more likely to mediate successful control of HIV infection1. Mutation within these epitopes can allow viral escape from CD8+ T-cell recognition. Here we analysed viral sequences and HLA alleles from >2,800 subjects, drawn from 9 distinct study cohorts spanning 5 continents. Initial analysis of the HLA-B*51-restricted epitope, TAFTIPSI (reverse transcriptase residues 128–135), showed a strong correlation between the frequency of the escape mutation I135X and HLA-B*51 prevalence in the 9 study cohorts (P = 0.0001). Extending these analyses to incorporate other well-defined CD8+ T-cell epitopes, including those restricted by HLA-B*57 and HLA-B*27, showed that the frequency of these epitope variants (n = 14) was consistently correlated with the prevalence of the restricting HLA allele in the different cohorts (together, P < 0.0001), demonstrating strong evidence of HIV adaptation to HLA at a population level. This process of viral adaptation may dismantle the well-established HLA associations with control of HIV infection that are linked to the availability of key epitopes, and highlights the challenge for a vaccine to keep pace with the changing immunological landscape presented by HIV.
