<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wang K</submitter><funding>Innovative Medicines Initiative</funding><funding>University of Alberta</funding><funding>Northern Alberta Clinical Trials and Research Centre</funding><funding>European Commission</funding><funding>Canadian Institutes of Health Research</funding><funding>Canada Research Chairs</funding><funding>European Federation of Pharmaceutical Industries and Associations</funding><funding>NEI NIH HHS</funding><funding>Horizon 2020 Framework Programme</funding><funding>T. Von Zastrow Foundation</funding><funding>Fundació la Marató de TV3</funding><funding>Österreichischen Akademie der Wissenschaften</funding><funding>Metabolomics Innovation Centre</funding><pagination>101254</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10694626</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4(11)</volume><pubmed_abstract>The post-acute sequelae of COVID-19 (PASC), also known as long COVID, is often associated with debilitating symptoms and adverse multisystem consequences. We obtain plasma samples from 117 individuals during and 6 months following their acute phase of infection to comprehensively profile and assess changes in cytokines, proteome, and metabolome. Network analysis reveals sustained inflammatory response, platelet degranulation, and cellular activation during convalescence accompanied by dysregulation in arginine biosynthesis, methionine metabolism, taurine metabolism, and tricarboxylic acid (TCA) cycle processes. Furthermore, we develop a prognostic model composed of 20 molecules involved in regulating T cell exhaustion and energy metabolism that can reliably predict adverse clinical outcome</pubmed_abstract><journal>Cell reports. Medicine</journal><pubmed_title>Sequential multi-omics analysis identifies clinical phenotypes and predictive biomarkers for long COVID.</pubmed_title><pmcid>PMC10694626</pmcid><funding_grant_id>F18-01336</funding_grant_id><funding_grant_id>101005026</funding_grant_id><funding_grant_id>F20–02343</funding_grant_id><funding_grant_id>F20-02015</funding_grant_id><funding_grant_id>P30 EY003039</funding_grant_id><funding_grant_id>RES50821</funding_grant_id><funding_grant_id>R01 EY025383</funding_grant_id><funding_grant_id>202125-31</funding_grant_id><pubmed_authors>Gordon PMK</pubmed_authors><pubmed_authors>Srinivasan K</pubmed_authors><pubmed_authors>Prasad V</pubmed_authors><pubmed_authors>Sligl W</pubmed_authors><pubmed_authors>Wishart DS</pubmed_authors><pubmed_authors>Khoramjoo M</pubmed_authors><pubmed_authors>Penninger JM</pubmed_authors><pubmed_authors>Wang K</pubmed_authors><pubmed_authors>Borchers CH</pubmed_authors><pubmed_authors>Jackson D</pubmed_authors><pubmed_authors>Grant MB</pubmed_authors><pubmed_authors>Mandal R</pubmed_authors><pubmed_authors>Oudit GY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sequential multi-omics analysis identifies clinical phenotypes and predictive biomarkers for long COVID.</name><description>The post-acute sequelae of COVID-19 (PASC), also known as long COVID, is often associated with debilitating symptoms and adverse multisystem consequences. We obtain plasma samples from 117 individuals during and 6 months following their acute phase of infection to comprehensively profile and assess changes in cytokines, proteome, and metabolome. Network analysis reveals sustained inflammatory response, platelet degranulation, and cellular activation during convalescence accompanied by dysregulation in arginine biosynthesis, methionine metabolism, taurine metabolism, and tricarboxylic acid (TCA) cycle processes. Furthermore, we develop a prognostic model composed of 20 molecules involved in regulating T cell exhaustion and energy metabolism that can reliably predict adverse clinical outcome</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2026-07-14T16:38:06.244Z</modification><creation>2026-06-21T03:07:31.211Z</creation></dates><accession>S-EPMC10694626</accession><cross_references><pubmed>37890487</pubmed><doi>10.1016/j.xcrm.2023.101254</doi></cross_references></HashMap>