{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo H"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","NCI NIH HHS","Division of Intramural Research, National Institute of Allergy and Infectious Diseases","U.S. Department of Health &amp; Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["423-433"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8087183"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(4)"],"pubmed_abstract":["Individuals infected with human immunodeficiency virus type-1 (HIV-1) show metabolic alterations of CD4<sup>+</sup> T cells through unclear mechanisms with undefined consequences. We analyzed the transcriptome of CD4<sup>+</sup> T cells from patients with HIV-1 and revealed that the elevated oxidative phosphorylation (OXPHOS) pathway is associated with poor outcomes. Inhibition of OXPHOS by the US Food and Drug Administration-approved drug metformin, which targets mitochondrial respiratory chain complex-I, suppresses HIV-1 replication in human CD4<sup>+</sup> T cells and humanized mice. In patients, HIV-1 peak viremia positively correlates with the expression of NLRX1, a mitochondrial innate immune receptor. Quantitative proteomics and metabolic analyses reveal that NLRX1 enhances OXPHOS a"],"journal":["Nature immunology"],"pubmed_title":["Multi-omics analyses reveal that HIV-1 alters CD4<sup>+</sup> T cell immunometabolism to fuel virus replication."],"pmcid":["PMC8087183"],"funding_grant_id":["P30 AI050410","U19 AI109965","P30 CA016086","R01 AI127346","DK119937","R01 AI138797","R01 DK119937","AI127346","R01 AI136990","P01 DK094779","R01 AI029564"],"pubmed_authors":["Holley-Guthrie E","Eller LA","Rampanelli E","Su L","Ting JP","Wang L","Garrido C","Margolis DM","Wang Q","Guo H","Ghneim K","Robb ML","Cheng L","Sekaly RP","Chen X"],"additional_accession":[]},"is_claimable":false,"name":"Multi-omics analyses reveal that HIV-1 alters CD4<sup>+</sup> T cell immunometabolism to fuel virus replication.","description":"Individuals infected with human immunodeficiency virus type-1 (HIV-1) show metabolic alterations of CD4<sup>+</sup> T cells through unclear mechanisms with undefined consequences. We analyzed the transcriptome of CD4<sup>+</sup> T cells from patients with HIV-1 and revealed that the elevated oxidative phosphorylation (OXPHOS) pathway is associated with poor outcomes. Inhibition of OXPHOS by the US Food and Drug Administration-approved drug metformin, which targets mitochondrial respiratory chain complex-I, suppresses HIV-1 replication in human CD4<sup>+</sup> T cells and humanized mice. In patients, HIV-1 peak viremia positively correlates with the expression of NLRX1, a mitochondrial innate immune receptor. Quantitative proteomics and metabolic analyses reveal that NLRX1 enhances OXPHOS a","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-05-01T12:55:47.445Z","creation":"2022-02-11T11:19:37.499Z"},"accession":"S-EPMC8087183","cross_references":{"pubmed":["33767427"],"doi":["10.1038/s41590-021-00898-1"]}}