{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T12:19:05Z","timestamp":1790857145176,"version":"4.1.0"},"reference-count":50,"publisher":"American Society for Microbiology","issue":"17","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Type I interferon (IFN-\u03b1\/\u03b2) comprises a family of immunomodulatory cytokines that are critical for controlling viral infections. In cell culture, many RNA viruses trigger IFN responses through the binding of RNA recognition molecules (RIG-I, MDA5, and TLR-3) and induction of interferon regulatory factor IRF-3-dependent gene transcription. Recent studies with West Nile virus (WNV) have shown that type I IFN is essential for restricting infection and that a deficiency of IRF-3 results in enhanced lethality. However, IRF-3 was not required for optimal systemic IFN production in vivo or in vitro in macrophages. To begin to define the transcriptional factors that regulate type I IFN after WNV infection, we evaluated IFN induction and virus control in IRF-7\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Compared to congenic wild-type mice, IRF-7\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed increased lethality after WNV infection and developed early and elevated WNV burdens in both peripheral and central nervous system tissues. As a correlate, a deficiency of IRF-7 blunted the systemic type I IFN response in mice. Consistent with this, IFN-\u03b1 gene expression and protein production were reduced and viral titers were increased in IRF-7\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    primary macrophages, fibroblasts, dendritic cells, and cortical neurons. In contrast, in these cells the IFN-\u03b2 response remained largely intact. Our data suggest that the early protective IFN-\u03b1 response against WNV occurs through an IRF-7-dependent transcriptional signal.\n                  <\/jats:p>","DOI":"10.1128\/jvi.00918-08","type":"journal-article","created":{"date-parts":[[2008,6,18]],"date-time":"2008-06-18T20:56:00Z","timestamp":1213822560000},"page":"8465-8475","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":147,"title":["Interferon Regulatory Factor IRF-7 Induces the Antiviral Alpha Interferon Response and Protects against Lethal West Nile Virus Infection"],"prefix":"10.1128","volume":"82","author":[{"given":"Stephane","family":"Daffis","sequence":"first","affiliation":[{"name":"Departments of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie A.","family":"Samuel","sequence":"additional","affiliation":[{"name":"Molecular Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mehul S.","family":"Suthar","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Washington School of Medicine, Seattle, Washington 98195-7650"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian C.","family":"Keller","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Washington School of Medicine, Seattle, Washington 98195-7650"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Michael","family":"Gale","sequence":"additional","affiliation":[{"name":"Department of Immunology, University of Washington School of Medicine, Seattle, Washington 98195-7650"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S.","family":"Diamond","sequence":"additional","affiliation":[{"name":"Departments of Medicine"},{"name":"Molecular Microbiology"},{"name":"Pathology &amp; Immunology, Washington University School of Medicine, St. Louis, Missouri 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