Fellay, JacquesShianna, Kevin V.Ge, DongliangColombo, SaraLedergerber, BrunoWeale, MikeZhang, KunlinGumbs, CurtisCastagna, AntonellaCossarizza, AndreaCozzi-Lepri, AlessandroDe Luca, AndreaEasterbrook, PhilippaFrancioli, PatrickMallal, SimonMartinez-Picado, JavierMiro, José M.Obel, NielsSmith, Jason P.Wyniger, JosianeDescombes, PatrickAntonarakis, Stylianos E.Letvin, Norman L.McMichael, Andrew J.Haynes, Barton F.Telenti, AmalioGoldstein, David B.2011-04-152011-04-152011-04-15200710.1126/science.1143767https://infoscience.epfl.ch/handle/20.500.14299/66444Understanding 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.Genome, Humantext::journal::journal article::research article