{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McLaren PJ"],"funding":["Swiss National Science Foundation","NIAID NIH HHS","Medical Research Council","NHLBI NIH HHS","NHGRI NIH HHS","NCI NIH HHS","Wellcome Trust"],"pagination":["1025-1030"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10848312"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["620(7976)"],"pubmed_abstract":["HIV-1 remains a global health crisis<sup>1</sup>, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa<sup>2</sup>, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV<sup>3</sup>. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log<sub>10</sub>-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC0"],"journal":["Nature"],"pubmed_title":["Africa-specific human genetic variation near CHD1L associates with HIV-1 load."],"pmcid":["PMC10848312"],"funding_grant_id":["MR/N02043X/1","UM1 AI068634","MR/S009752/1","U54 AI170792","UM1 AI068636","75N91019D00024","U01 AI035039","U01 HL146208","201369","220740/Z/20/Z","U01 HL146240","U01 HL146201","U01 HL146333","MC_UU_00033/1","R01 AI165236","U24 HG006941","197721","MC_UU_00033/3","P30 AI117943"],"pubmed_authors":["Kilembe W","Bassett A","Skarnes WC","Wolinsky SM","Herbeck JT","Porter T","Theodorou I","Kaleebu P","Kral AH","Iaconis G","Mullins JI","Fatumo S","Trkola A","Haas DW","Angelino P","Simons LM","De Luca A","Lever AML","Jarvis I","Kootstra NA","Goedert JJ","Bartha I","Winkler CA","Rauch A","Kiar CS","Carrington M","Meyer L","Walter M","Miro JM","Pirie F","Mok HP","Kim EY","Bashirova A","Dougan G","Mallal S","Johnson EO","Mukhopadhyay S","Gurdasani D","Thorball CW","Walker BD","Montgomery SB","Goldstein DB","McLaren PJ","Zagury JF","Moodley P","Cossarizza A","Poli G","Fellay J","Price MA","Karakoc E","Nam K","Martinez-Picado J","Tough RH","Tuff JF","Hultquist JF","Ciuffi A","Obel N","Cristinelli S","Lambotte O","Kirk GD","Motala AA","Plummer FA","Pomilla C","DeGorter MK","Luo M","Sandhu MS","Sathya Moorthy MP","Buchbinder S","Groom H","Porreca I","Carstensen T"],"additional_accession":[]},"is_claimable":false,"name":"Africa-specific human genetic variation near CHD1L associates with HIV-1 load.","description":"HIV-1 remains a global health crisis<sup>1</sup>, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa<sup>2</sup>, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV<sup>3</sup>. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log<sub>10</sub>-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC0","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2026-03-17T15:20:54.441Z","creation":"2025-02-18T23:24:25.587Z"},"accession":"S-EPMC10848312","cross_references":{"pubmed":["37532928"],"doi":["10.1038/s41586-023-06370-4"]}}