<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lopez Angel CJ</submitter><funding>HHS | National Institutes of Health</funding><pagination>e2022928118</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8040665</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>118(14)</volume><pubmed_abstract>Chronic inflammation is thought to be a major cause of morbidity and mortality in aging, but whether similar mechanisms underlie dysfunction in infection-associated chronic inflammation is unclear. Here, we profiled the immune proteome, and cellular composition and signaling states in a cohort of aging individuals versus a set of HIV patients on long-term antiretroviral therapy therapy or hepatitis C virus (HCV) patients before and after sofosbuvir treatment. We found shared alterations in aging-associated and infection-associated chronic inflammation including T cell memory inflation, up-regulation of intracellular signaling pathways of inflammation, and diminished sensitivity to cytokines in lymphocytes and myeloid cells. In the HIV cohort, these dysregulations were evident despite viral</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Signatures of immune dysfunction in HIV and HCV infection share features with chronic inflammation in aging and persist after viral reduction or elimination.</pubmed_title><pmcid>PMC8040665</pmcid><funding_grant_id>U19 AI057229</funding_grant_id><pubmed_authors>Rosenberg-Hasson Y</pubmed_authors><pubmed_authors>Lopez Angel CJ</pubmed_authors><pubmed_authors>Dekker CL</pubmed_authors><pubmed_authors>Grant PM</pubmed_authors><pubmed_authors>Nguyen T</pubmed_authors><pubmed_authors>Glenn JS</pubmed_authors><pubmed_authors>Vallania F</pubmed_authors><pubmed_authors>Khatri P</pubmed_authors><pubmed_authors>Pham EA</pubmed_authors><pubmed_authors>Fram BJ</pubmed_authors><pubmed_authors>Maecker HT</pubmed_authors><pubmed_authors>Du H</pubmed_authors><pubmed_authors>Davis MM</pubmed_authors><pubmed_authors>Ahmed A</pubmed_authors><pubmed_authors>Furman D</pubmed_authors><pubmed_authors>Perez K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Signatures of immune dysfunction in HIV and HCV infection share features with chronic inflammation in aging and persist after viral reduction or elimination.</name><description>Chronic inflammation is thought to be a major cause of morbidity and mortality in aging, but whether similar mechanisms underlie dysfunction in infection-associated chronic inflammation is unclear. Here, we profiled the immune proteome, and cellular composition and signaling states in a cohort of aging individuals versus a set of HIV patients on long-term antiretroviral therapy therapy or hepatitis C virus (HCV) patients before and after sofosbuvir treatment. We found shared alterations in aging-associated and infection-associated chronic inflammation including T cell memory inflation, up-regulation of intracellular signaling pathways of inflammation, and diminished sensitivity to cytokines in lymphocytes and myeloid cells. In the HIV cohort, these dysregulations were evident despite viral</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-26T08:17:16.367Z</modification><creation>2022-02-09T15:32:53.425Z</creation></dates><accession>S-EPMC8040665</accession><cross_references><pubmed>33811141</pubmed><doi>10.1073/pnas.2022928118</doi></cross_references></HashMap>