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Clinically relevant animal models of NHV-induced hepatitis are limited, contributing to the incomplete understanding of pathological mechanisms. Murine norovirus (MNV) elicits hepatosplenomegaly in mice lacking the antiviral immune effector Signal Transducer and Activator of Transcription-1 (STAT1), providing a model to investigate mechanisms of NHV-induced hepatic pathology.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>\n                    STAT1-sufficient and -deficient (\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>Het<\/jats:sup>\n                    ,\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>KO<\/jats:sup>\n                    ) littermates infected intravenously (i.v.) with MNV strain CR6 were assessed for hepatic inflammation and viral burden. Cell types and molecular pathways associated with hepatic pathology in CR6-infected\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>KO<\/jats:sup>\n                    mice were identified by flow cytometry and RNAseq of liver tissue. The relative importance of hematopoietic vs non-hematopoietic expression of STAT1 in restricting CR6 replication and maintaining tissue homeostasis was assessed in bone marrow chimeras.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    MNV CR6\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>KO<\/jats:sup>\n                    mice developed severe hepatitis with patchy hepatocellular necrosis and localized enrichment of CR6-infected myeloid cells, particularly macrophages. Gene set enrichment analysis (GSEA) of hepatic biopsies isolated from CR6-infected\n                    <jats:italic>Stat1<\/jats:italic>\n                    <jats:sup>KO<\/jats:sup>\n                    mice suggested dysregulated myeloid cell activation and indicated similarities between murine and human hepatic pathologies. STAT1 expression in hematopoietic cells was protective against hepatic viral dissemination, but hematopoietic STAT1-deficiency permitted persistent hepatic MNV infection, facilitating dysregulated myeloid cell activation and hepatic fibrosis.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>These results demonstrate that the role of STAT1 extends beyond restricting MNV dissemination and suggest that STAT1-dependent regulation of myeloid cell activation prevents acute hepatic necroinflammation and secondary fibrosis. This model of MNV-induced hepatitis may prove valuable in elucidating mechanisms of rare clinical complications.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Synopsis<\/jats:title>\n                  <jats:p>Mechanisms driving acute hepatitis caused by non-hepatotropic viruses are not well understood. We describe a model of non-hepatotropic murine norovirus infection that reliably induces liver pathology and identify a requirement for STAT1 expression in myeloid cells to promote antiviral immunity and hepatic tissue protection.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Graphical Abstract<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"720966v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                <\/jats:sec>","DOI":"10.64898\/2026.04.26.720966","type":"posted-content","created":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T01:14:02Z","timestamp":1777511642000},"source":"Crossref","is-referenced-by-count":0,"title":["STAT1 expression in myeloid cells restrains murine norovirus-induced hepatitis and fibrosis"],"prefix":"10.64898","author":[{"given":"Andrew J","family":"Sharon","sequence":"first","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madilyn B","family":"Portas","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasmine","family":"Wright","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harshad","family":"Ingle","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blair K","family":"Hardman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin J","family":"Goldberg","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jung Hee","family":"Seo","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ninan","family":"Abraham","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc S","family":"Horwitz","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan T","family":"Baldridge","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blayne A","family":"Sayed","sequence":"additional","affiliation":[{"name":"Division of General Surgery, Department of Surgery, University of Toronto, Toronto, Ontario, Canada"},{"name":"Cell and Systems Biology Program, The Hospital for Sick Children Research Institute, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa C","family":"Osborne","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Life Sciences Institute, University of British Columbia, Vancouver BC Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026050722185913000_2026.04.26.720966v1.1","doi-asserted-by":"crossref","unstructured":"Ray G . 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