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