{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu X"],"funding":["HHS | National Institutes of Health","Bayerisches Staatsministerium für Bildung und Kultus, Wissenschaft und Kunst","The institute for Basic science, Korea","NIDCR NIH HHS","KRIBB, Korea","NIAID NIH HHS","NCI NIH HHS"],"pagination":["e0040222"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9040823"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(2)"],"pubmed_abstract":["Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers cytokine-mediated inflammation, leading to a myriad of clinical presentations in COVID-19. The SARS-CoV-2 open reading frame 8 (ORF8) is a secreted and rapidly evolving glycoprotein. Patients infected with SARS-CoV-2 variants with ORF8 deleted are associated with mild disease outcomes, but the molecular mechanism behind this is unknown. Here, we report that SARS-CoV-2 ORF8 is a viral cytokine that is similar to but distinct from interleukin 17A (IL-17A) as it induces stronger and broader human IL-17 receptor (hIL-17R) signaling than IL-17A. ORF8 primarily targeted blood monocytes and induced the heterodimerization of hIL-17RA and hIL-17RC, triggering a robust inflammatory response. Transcriptome analysis reveal"],"journal":["mBio"],"pubmed_title":["Viral Mimicry of Interleukin-17A by SARS-CoV-2 ORF8."],"pmcid":["PMC9040823"],"funding_grant_id":["BMBF SenseCoV2 01KI20172A","DE027888","R35 CA200422","R01 DE028521","R01 AI140705","R01 AI140718","R01 CA251275","AI152190","CA200422","K99 DE028573","DE023926","AI140705","KGM9942011","IBS-R801-D1","R00 DE028573","CA251275","R01 AI152190","AI140705S1","R21 DE027888","AI140718","DE028521","R01 DE023926","DFG Fokus COVID-19 EN423/7-1","K99DE028573"],"pubmed_authors":["Poo H","Herrmann A","Xia T","Shin WJ","Jehi L","Zhang P","Lee JS","Jung W","Choi YK","Jung JU","Ensser A","Foo SS","Chen W","Comhair SAA","Yu KM","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"Viral Mimicry of Interleukin-17A by SARS-CoV-2 ORF8.","description":"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection triggers cytokine-mediated inflammation, leading to a myriad of clinical presentations in COVID-19. The SARS-CoV-2 open reading frame 8 (ORF8) is a secreted and rapidly evolving glycoprotein. Patients infected with SARS-CoV-2 variants with ORF8 deleted are associated with mild disease outcomes, but the molecular mechanism behind this is unknown. Here, we report that SARS-CoV-2 ORF8 is a viral cytokine that is similar to but distinct from interleukin 17A (IL-17A) as it induces stronger and broader human IL-17 receptor (hIL-17R) signaling than IL-17A. ORF8 primarily targeted blood monocytes and induced the heterodimerization of hIL-17RA and hIL-17RC, triggering a robust inflammatory response. Transcriptome analysis reveal","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-06-07T03:18:42.813Z","creation":"2025-04-20T03:08:12.831Z"},"accession":"S-EPMC9040823","cross_references":{"pubmed":["35343786"],"doi":["10.1128/mbio.00402-22"]}}