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