| Literature DB >> 17641165 |
Jacques Fellay1, Kevin V Shianna, Dongliang Ge, Sara Colombo, Bruno Ledergerber, Mike Weale, Kunlin Zhang, Curtis Gumbs, Antonella Castagna, Andrea Cossarizza, Alessandro Cozzi-Lepri, Andrea De Luca, Philippa Easterbrook, Patrick Francioli, Simon Mallal, Javier Martinez-Picado, José M Miro, Niels Obel, Jason P Smith, Josiane Wyniger, Patrick Descombes, Stylianos E Antonarakis, Norman L Letvin, Andrew J McMichael, Barton F Haynes, Amalio Telenti, David B Goldstein.
Abstract
Understanding why some people establish and maintain effective control of HIV-1 and others do not is a priority in the effort to develop new treatments for HIV/AIDS. Using a whole-genome association strategy, we identified polymorphisms that explain nearly 15% of the variation among individuals in viral load during the asymptomatic set-point period of infection. One of these is found within an endogenous retroviral element and is associated with major histocompatibility allele human leukocyte antigen (HLA)-B*5701, whereas a second is located near the HLA-C gene. An additional analysis of the time to HIV disease progression implicated two genes, one of which encodes an RNA polymerase I subunit. These findings emphasize the importance of studying human genetic variation as a guide to combating infectious agents.Entities:
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Year: 2007 PMID： 17641165 PMCID： PMC1991296 DOI： 10.1126/science.1143767
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728