{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Scoon WA"],"funding":["NCATS NIH HHS","Howard Hughes Medical Institute","NIAID NIH HHS","NHLBI NIH HHS"],"pagination":["2286-2302"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9561183"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(10)"],"pubmed_abstract":["Liver damage and an exacerbated inflammatory response are hallmarks of Ebola virus (EBOV) infection. Little is known about the intrinsic response to infection in human hepatocytes and their contribution to inflammation. Here, we present an induced pluripotent stem cell (iPSC)-derived hepatocyte-like cell (HLC) platform to define the hepato-intrinsic response to EBOV infection. We used this platform to show robust EBOV infection, with characteristic ultrastructural changes and evidence for viral replication. Transcriptomics analysis revealed a delayed response with minimal early transcriptomic changes, followed by a general downregulation of hepatic function and upregulation of interferon signaling, providing a potential mechanism by which hepatocytes participate in disease severity and liv"],"journal":["Stem cell reports"],"pubmed_title":["Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes."],"pmcid":["PMC9561183"],"funding_grant_id":["R21 AI137793","TL1 TR001410","T32 HL007035","R21 AI135912","R01 AI133486"],"pubmed_authors":["Wilson AA","Muhlberger E","Mazur S","Flores EY","Wang F","Mostoslavsky G","Lindstrom-Vautrin J","Olejnik J","Bhatia SN","Scoon WA","Villacorta-Martin C","March-Riera S","Bernbaum JG","Hume AJ","Mancio-Silva L","Kaserman JE","Johnson RF","Suder EL","Mithal A"],"additional_accession":[]},"is_claimable":false,"name":"Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes.","description":"Liver damage and an exacerbated inflammatory response are hallmarks of Ebola virus (EBOV) infection. Little is known about the intrinsic response to infection in human hepatocytes and their contribution to inflammation. Here, we present an induced pluripotent stem cell (iPSC)-derived hepatocyte-like cell (HLC) platform to define the hepato-intrinsic response to EBOV infection. We used this platform to show robust EBOV infection, with characteristic ultrastructural changes and evidence for viral replication. Transcriptomics analysis revealed a delayed response with minimal early transcriptomic changes, followed by a general downregulation of hepatic function and upregulation of interferon signaling, providing a potential mechanism by which hepatocytes participate in disease severity and liv","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2026-05-28T04:42:09.769Z","creation":"2024-11-21T06:46:23.423Z"},"accession":"S-EPMC9561183","cross_references":{"pubmed":["36084636"],"doi":["10.1016/j.stemcr.2022.08.003"]}}