<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee GQ</submitter><funding>Michael Smith Foundation for Health Research (MSFHR)</funding><funding>NIAID NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Institute of Allergy and Infectious Diseases</funding><funding>Michael Smith Foundation for Health Research</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID)</funding><funding>Wellcome Trust</funding><funding>Gouvernement du Canada | Canadian Institutes of Health Research</funding><funding>Division of Intramural Research, National Institute of Allergy and Infectious Diseases</funding><funding>Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada)</funding><funding>Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID)</funding><pagination>5480</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11219899</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>The primary obstacle to curing HIV-1 is a reservoir of CD4+ cells that contain stably integrated provirus. Previous studies characterizing the proviral landscape, which have been predominantly conducted in males in the United States and Europe living with HIV-1 subtype B, have revealed that most proviruses that persist during antiretroviral therapy (ART) are defective. In contrast, less is known about proviral landscapes in females with non-B subtypes, which represents the largest group of individuals living with HIV-1. Here, we analyze genomic DNA from resting CD4+ T-cells from 16 female and seven male Ugandans with HIV-1 receiving suppressive ART (n = 23). We perform near-full-length proviral sequencing at limiting dilution to examine the proviral genetic landscape, yielding 607 HIV-1 su</pubmed_abstract><journal>Nature communications</journal><pubmed_title>HIV-1 subtype A1, D, and recombinant proviral genome landscapes during long-term suppressive therapy.</pubmed_title><pmcid>PMC11219899</pmcid><funding_grant_id>CGS-M awards</funding_grant_id><funding_grant_id>Canada Research Chairs Program</funding_grant_id><funding_grant_id>UM1AI164565</funding_grant_id><funding_grant_id>Vanier Canada Graduate Scholarship</funding_grant_id><funding_grant_id>107752/Z/15/Z</funding_grant_id><funding_grant_id>PJT-159625</funding_grant_id><funding_grant_id>Scholar Award</funding_grant_id><funding_grant_id>UM1 AI164565</funding_grant_id><funding_grant_id>NA</funding_grant_id><funding_grant_id>R21AI150398</funding_grant_id><funding_grant_id>R21 AI150398</funding_grant_id><funding_grant_id>R01 AI162221</funding_grant_id><funding_grant_id>R01AI162221</funding_grant_id><pubmed_authors>Brumme ZL</pubmed_authors><pubmed_authors>Prodger JL</pubmed_authors><pubmed_authors>Gowanlock SN</pubmed_authors><pubmed_authors>Anok A</pubmed_authors><pubmed_authors>Kityamuweesi T</pubmed_authors><pubmed_authors>Reynolds SJ</pubmed_authors><pubmed_authors>Kinloch NN</pubmed_authors><pubmed_authors>Kasule J</pubmed_authors><pubmed_authors>Buule P</pubmed_authors><pubmed_authors>Tomusange S</pubmed_authors><pubmed_authors>Quinn TC</pubmed_authors><pubmed_authors>Lee GQ</pubmed_authors><pubmed_authors>Galiwango RM</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Copertino DC</pubmed_authors><pubmed_authors>Redd AD</pubmed_authors><pubmed_authors>Omondi FH</pubmed_authors><pubmed_authors>Jamiru S</pubmed_authors><pubmed_authors>Jones RB</pubmed_authors><pubmed_authors>Duncan MC</pubmed_authors><pubmed_authors>Khadka P</pubmed_authors></additional><is_claimable>false</is_claimable><name>HIV-1 subtype A1, D, and recombinant proviral genome landscapes during long-term suppressive therapy.</name><description>The primary obstacle to curing HIV-1 is a reservoir of CD4+ cells that contain stably integrated provirus. Previous studies characterizing the proviral landscape, which have been predominantly conducted in males in the United States and Europe living with HIV-1 subtype B, have revealed that most proviruses that persist during antiretroviral therapy (ART) are defective. In contrast, less is known about proviral landscapes in females with non-B subtypes, which represents the largest group of individuals living with HIV-1. Here, we analyze genomic DNA from resting CD4+ T-cells from 16 female and seven male Ugandans with HIV-1 receiving suppressive ART (n = 23). We perform near-full-length proviral sequencing at limiting dilution to examine the proviral genetic landscape, yielding 607 HIV-1 su</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-07-15T08:23:16.399Z</modification><creation>2025-04-04T12:21:09.122Z</creation></dates><accession>S-EPMC11219899</accession><cross_references><pubmed>38956017</pubmed><doi>10.1038/s41467-024-48985-9</doi></cross_references></HashMap>