<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang Z</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NIMHD NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>1081-1093</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9339474</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(8)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Alterations in gut microbiota and blood metabolomic profiles have been implicated in HIV infection and cardiovascular disease. However, it remains unclear whether alterations in gut microbiota may contribute to disrupted host blood metabolomic profiles in relation to atherosclerosis, especially in the context of HIV infection.&lt;h4>Methods&lt;/h4>We analyzed cross-sectional associations between gut microbiota features and carotid artery plaque in 361 women with or at high risk of HIV (67% HIV+), and further integrated plaque-associated microbial features with plasma lipidomic/metabolomic profiles. Furthermore, in 737 women and men, we examined prospective associations of baseline gut bacteria-associated lipidomic and metabolomic profiles with incident carotid artery plaque ov</pubmed_abstract><journal>Arteriosclerosis, thrombosis, and vascular biology</journal><pubmed_title>Gut Microbiota, Plasma Metabolomic Profiles, and Carotid Artery Atherosclerosis in HIV Infection.</pubmed_title><pmcid>PMC9339474</pmcid><funding_grant_id>P30 AI050410</funding_grant_id><funding_grant_id>K01 HL129892</funding_grant_id><funding_grant_id>UL1 TR001881</funding_grant_id><funding_grant_id>U01 AI035004</funding_grant_id><funding_grant_id>U01 HL146205</funding_grant_id><funding_grant_id>U01 HL146204</funding_grant_id><funding_grant_id>U01 HL146203</funding_grant_id><funding_grant_id>U01 HL146208</funding_grant_id><funding_grant_id>P30 AI124414</funding_grant_id><funding_grant_id>U01 HL146242</funding_grant_id><funding_grant_id>R01 MD011389</funding_grant_id><funding_grant_id>U01 HL146241</funding_grant_id><funding_grant_id>U01 HL146240</funding_grant_id><funding_grant_id>P30 CA013330</funding_grant_id><funding_grant_id>U01 HL146202</funding_grant_id><funding_grant_id>U01 HL146245</funding_grant_id><funding_grant_id>U01 HL146201</funding_grant_id><funding_grant_id>R01 HL140976</funding_grant_id><funding_grant_id>R01 HL126543</funding_grant_id><funding_grant_id>P30 MH116867</funding_grant_id><funding_grant_id>P30 DK040561</funding_grant_id><funding_grant_id>P30 AI073961</funding_grant_id><funding_grant_id>P30 AI027767</funding_grant_id><funding_grant_id>UL1 TR003098</funding_grant_id><funding_grant_id>R01 HL132794</funding_grant_id><funding_grant_id>R01 HL095140</funding_grant_id><funding_grant_id>U01 AI031834</funding_grant_id><funding_grant_id>UL1 TR000004</funding_grant_id><funding_grant_id>P30 AI050409</funding_grant_id><funding_grant_id>U01 HL146333</funding_grant_id><funding_grant_id>U01 HL146194</funding_grant_id><funding_grant_id>U01 HL146193</funding_grant_id><funding_grant_id>U01 HL146192</funding_grant_id><funding_grant_id>R01 HL083760</funding_grant_id><pubmed_authors>Malvestutto C</pubmed_authors><pubmed_authors>Wolinsky SM</pubmed_authors><pubmed_authors>Clish CB</pubmed_authors><pubmed_authors>Aouizerat B</pubmed_authors><pubmed_authors>Golub ET</pubmed_authors><pubmed_authors>Qi Q</pubmed_authors><pubmed_authors>Xing J</pubmed_authors><pubmed_authors>Sharma A</pubmed_authors><pubmed_authors>Anastos K</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Peters BA</pubmed_authors><pubmed_authors>Post WS</pubmed_authors><pubmed_authors>Budoff M</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors><pubmed_authors>Kassaye S</pubmed_authors><pubmed_authors>Burk RD</pubmed_authors><pubmed_authors>Weber K</pubmed_authors><pubmed_authors>Usyk M</pubmed_authors><pubmed_authors>Lazar J</pubmed_authors><pubmed_authors>Landay AL</pubmed_authors><pubmed_authors>French A</pubmed_authors><pubmed_authors>Gustafson D</pubmed_authors><pubmed_authors>Hanna DB</pubmed_authors><pubmed_authors>Hodis HN</pubmed_authors><pubmed_authors>Haberlen S</pubmed_authors><pubmed_authors>Kaplan RC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Gut Microbiota, Plasma Metabolomic Profiles, and Carotid Artery Atherosclerosis in HIV Infection.</name><description>&lt;h4>Background&lt;/h4>Alterations in gut microbiota and blood metabolomic profiles have been implicated in HIV infection and cardiovascular disease. However, it remains unclear whether alterations in gut microbiota may contribute to disrupted host blood metabolomic profiles in relation to atherosclerosis, especially in the context of HIV infection.&lt;h4>Methods&lt;/h4>We analyzed cross-sectional associations between gut microbiota features and carotid artery plaque in 361 women with or at high risk of HIV (67% HIV+), and further integrated plaque-associated microbial features with plasma lipidomic/metabolomic profiles. Furthermore, in 737 women and men, we examined prospective associations of baseline gut bacteria-associated lipidomic and metabolomic profiles with incident carotid artery plaque ov</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Aug</publication><modification>2025-04-04T20:07:33.08Z</modification><creation>2025-04-04T20:07:33.08Z</creation></dates><accession>S-EPMC9339474</accession><cross_references><pubmed>35678187</pubmed><doi>10.1161/ATVBAHA.121.317276</doi><doi>10.1161/atvbaha.121.317276</doi></cross_references></HashMap>