{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Angioni R"],"funding":["Fondazione Città della Speranza"],"pagination":["101266"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10694673"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(11)"],"pubmed_abstract":["The spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has fueled the COVID-19 pandemic with its enduring medical and socioeconomic challenges because of subsequent waves and long-term consequences of great concern. Here, we chart the molecular basis of COVID-19 pathogenesis by analyzing patients' immune responses at single-cell resolution across disease course and severity. This approach confirms cell subpopulation-specific dysregulation in COVID-19 across disease course and severity and identifies a severity-associated activation of the receptor for advanced glycation endproducts (RAGE) pathway in monocytes. In vitro THP1-based experiments indicate that monocytes bind the SARS-CoV-2 S1-receptor binding domain (RBD) via RAGE, pointing to RAGE-Spike interaction enabling monocyte infection. Thus, our results demonstrate that RAGE is a functional receptor of SARS-CoV-2 contributing to COVID-19 severity."],"journal":["Cell reports. Medicine"],"pubmed_title":["RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity."],"pmcid":["PMC10694673"],"funding_grant_id":["20/02CoV"],"pubmed_authors":["Viola A","Pasqualato S","Buratto D","Elli F","Rotta L","Scardua A","Zonta F","Bonfanti M","Savino A","Cattelan AM","Caporale N","Ghezzi S","Ferrari P","Molon B","Putaggio C","Sanchez-Rodriguez R","Ricciardelli E","Pagani I","Bertoldi N","Weber J","Villa CE","Munari F","Vicenzi E","Zanon C","Iorio F","Angioni R","Cecatiello V","Vannini A","Testa G"],"additional_accession":[]},"is_claimable":false,"name":"RAGE engagement by SARS-CoV-2 enables monocyte infection and underlies COVID-19 severity.","description":"The spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has fueled the COVID-19 pandemic with its enduring medical and socioeconomic challenges because of subsequent waves and long-term consequences of great concern. Here, we chart the molecular basis of COVID-19 pathogenesis by analyzing patients' immune responses at single-cell resolution across disease course and severity. This approach confirms cell subpopulation-specific dysregulation in COVID-19 across disease course and severity and identifies a severity-associated activation of the receptor for advanced glycation endproducts (RAGE) pathway in monocytes. In vitro THP1-based experiments indicate that monocytes bind the SARS-CoV-2 S1-receptor binding domain (RBD) via RAGE, pointing to RAGE-Spike interaction enabling monocyte infection. Thus, our results demonstrate that RAGE is a functional receptor of SARS-CoV-2 contributing to COVID-19 severity.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2026-05-28T08:59:55.83Z","creation":"2025-02-19T04:25:41.579Z"},"accession":"S-EPMC10694673","cross_references":{"pubmed":["37944530"],"doi":["10.1016/j.xcrm.2023.101266"]}}