{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fellay J"],"funding":["NIAID NIH HHS","Medical Research Council"],"pagination":["944-7"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC1991296"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["317(5840)"],"pubmed_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 combati"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["A whole-genome association study of major determinants for host control of HIV-1."],"pmcid":["PMC1991296"],"funding_grant_id":["U19 AI067854-03","G0200585","MC_U137884177","U19 AI067854"],"pubmed_authors":["Ge D","Zhang K","Easterbrook P","Wyniger J","Goldstein DB","Francioli P","Cossarizza A","Letvin NL","Fellay J","Haynes BF","Cozzi-Lepri A","Castagna A","De Luca A","Martinez-Picado J","Descombes P","Ledergerber B","Obel N","Smith JP","Miro JM","Antonarakis SE","Shianna KV","Mallal S","McMichael AJ","Telenti A","Weale M","Colombo S","Gumbs C"],"additional_accession":[]},"is_claimable":false,"name":"A whole-genome association study of major determinants for host control of HIV-1.","description":"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 combati","dates":{"release":"2007-01-01T00:00:00Z","publication":"2007 Aug","modification":"2025-04-03T22:52:21.77Z","creation":"2019-06-06T15:22:47Z"},"accession":"S-EPMC1991296","cross_references":{"pubmed":["17641165"],"doi":["10.1126/science.1143767"]}}