<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Schank M</submitter><funding>NIH HHS</funding><pagination>1061</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10224005</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(5)</volume><pubmed_abstract>We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate the mechanism(s) of CD4 T cell mitochondrial compromise in ART-controlled PLWH. We first assessed the levels of reactive oxygen species (ROS), and we observed significantly increased cellular and mitochondrial ROS levels in CD4 T cells from PLWH compared to healthy subjects (HS). Furthermore, we observed a significant reduction in the levels of proteins responsible for antioxidant defense (superoxide dismutase 1, SOD1) and ROS-mediated DNA damage repair (apurinic/apyrimidinic endonuclease</pubmed_abstract><journal>Viruses</journal><pubmed_title>ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.</pubmed_title><pmcid>PMC10224005</pmcid><funding_grant_id>R21AI157909</funding_grant_id><funding_grant_id>R15AG069544</funding_grant_id><funding_grant_id>R15AG076370-01</funding_grant_id><funding_grant_id>R15AG076370-015S1</funding_grant_id><pubmed_authors>Jiang Y</pubmed_authors><pubmed_authors>El Gazzar M</pubmed_authors><pubmed_authors>Ning S</pubmed_authors><pubmed_authors>Nguyen LNT</pubmed_authors><pubmed_authors>Moorman JP</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Yao ZQ</pubmed_authors><pubmed_authors>Wu XY</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors><pubmed_authors>Schank M</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.</name><description>We have previously demonstrated mitochondrial dysfunction in aging CD4 T cells from antiretroviral therapy (ART)-controlled people living with HIV (PLWH). However, the underlying mechanisms by which CD4 T cells develop mitochondrial dysfunction in PLWH remain unclear. In this study, we sought to elucidate the mechanism(s) of CD4 T cell mitochondrial compromise in ART-controlled PLWH. We first assessed the levels of reactive oxygen species (ROS), and we observed significantly increased cellular and mitochondrial ROS levels in CD4 T cells from PLWH compared to healthy subjects (HS). Furthermore, we observed a significant reduction in the levels of proteins responsible for antioxidant defense (superoxide dismutase 1, SOD1) and ROS-mediated DNA damage repair (apurinic/apyrimidinic endonuclease</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2025-05-29T16:22:29.539Z</modification><creation>2025-05-29T16:22:29.539Z</creation></dates><accession>S-EPMC10224005</accession><cross_references><pubmed>37243148</pubmed><doi>10.3390/v15051061</doi></cross_references></HashMap>