<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Grosgebauer K</submitter><funding>National Institute of Allergy and Infectious Diseases</funding><funding>NIDA NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>State of Florida</funding><funding>National Institute on Drug Abuse</funding><pagination>16-22</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6347547</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>This cross-sectional study investigated the associations of psychosocial factors relevant to recovery from substance use disorders with monocyte activation and HIV persistence in a sample of 84 HIV-positive, methamphetamine-using sexual minority men with undetectable HIV viral load (&lt;40 copies/mL). We examined if psychosocial factors were associated with decreased soluble CD14 (sCD14) and lower proviral HIV DNA. Multiple linear regression models adjusted for age, anti-retroviral therapy regimen, and CD4+ T-cell count. Time on ART was also included in models examining proviral HIV DNA. Greater self-efficacy for managing methamphetamine triggers and higher social support for abstinence were independently associated with lower sCD14. Greater social support for abstinence was also independently associated with lower proviral HIV DNA. Psychosocial factors relevant to recovery from substance use disorders are associated with lower monocyte activation and decreased proviral HIV DNA. Findings underscore the need for longitudinal research to identify plausible mechanisms linking psychosocial factors and substance use with biological processes relevant to HIV pathogenesis.</pubmed_abstract><journal>Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology</journal><pubmed_title>Psychosocial Correlates of Monocyte Activation and HIV Persistence in Methamphetamine Users.</pubmed_title><pmcid>PMC6347547</pmcid><funding_grant_id>P30-AI027763</funding_grant_id><funding_grant_id>P30 AI073961</funding_grant_id><funding_grant_id>P30 AI027763</funding_grant_id><funding_grant_id>R01 DA033854</funding_grant_id><funding_grant_id>P30-AI073961</funding_grant_id><funding_grant_id>R01-DA033854</funding_grant_id><pubmed_authors>Grosgebauer K</pubmed_authors><pubmed_authors>Dilworth SE</pubmed_authors><pubmed_authors>Salinas J</pubmed_authors><pubmed_authors>Sharkey M</pubmed_authors><pubmed_authors>Roach M</pubmed_authors><pubmed_authors>Carrico AW</pubmed_authors><pubmed_authors>Koru-Sengul T</pubmed_authors><pubmed_authors>Pallikkuth S</pubmed_authors><pubmed_authors>Pahwa S</pubmed_authors><pubmed_authors>Stevenson M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Psychosocial Correlates of Monocyte Activation and HIV Persistence in Methamphetamine Users.</name><description>This cross-sectional study investigated the associations of psychosocial factors relevant to recovery from substance use disorders with monocyte activation and HIV persistence in a sample of 84 HIV-positive, methamphetamine-using sexual minority men with undetectable HIV viral load (&lt;40 copies/mL). We examined if psychosocial factors were associated with decreased soluble CD14 (sCD14) and lower proviral HIV DNA. Multiple linear regression models adjusted for age, anti-retroviral therapy regimen, and CD4+ T-cell count. Time on ART was also included in models examining proviral HIV DNA. Greater self-efficacy for managing methamphetamine triggers and higher social support for abstinence were independently associated with lower sCD14. Greater social support for abstinence was also independently associated with lower proviral HIV DNA. Psychosocial factors relevant to recovery from substance use disorders are associated with lower monocyte activation and decreased proviral HIV DNA. Findings underscore the need for longitudinal research to identify plausible mechanisms linking psychosocial factors and substance use with biological processes relevant to HIV pathogenesis.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Mar</publication><modification>2024-10-18T12:19:21.192Z</modification><creation>2020-05-22T11:35:17Z</creation></dates><accession>S-EPMC6347547</accession><cross_references><pubmed>30046962</pubmed><doi>10.1007/s11481-018-9797-2</doi></cross_references></HashMap>