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The studies presented here evaluated the requirements for functional IFN receptors and the IFN signaling molecule STAT1 in IFN-\u03b1\/\u03b2 induction during infections of mice with lymphocytic choriomeningitis virus (LCMV). At 24 h after infection, levels of induced IFN-\u03b1\/\u03b2 in serum were reduced 90 to 95% in IFN-\u03b1\/\u03b2 receptor-deficient (IFN-\u03b1\/\u03b2R<jats:sup>\u2212\/\u2212<\/jats:sup>) and STAT1<jats:sup>\u2212\/\u2212<\/jats:sup>mice compared to those in wild-type mice. However, at 48 h, these mice showed elevated expression in the serum whereas IFN-\u03b1\/\u03b2 levels were still reduced &gt;75% in IFN-\u03b1\/\u03b2\u03b3R<jats:sup>\u2212\/\u2212<\/jats:sup>mice even though the viral burden was heavy. Levels of IFN-\u03b2, IFN-\u03b14, and non-IFN-\u03b14 subtype mRNA expression correlated with IFN-\u03b1\/\u03b2 bioactivity, and all IFN-\u03b1\/\u03b2 subtypes were coincidentally detectable. IRF-7 mRNA was induced under conditions of IFN-\u03b1\/\u03b2 production, including late production in IFN-\u03b1\/\u03b2R<jats:sup>\u2212\/\u2212<\/jats:sup>mice. These data demonstrate that the presence of the virus alone is not sufficient to induce IFN-\u03b1\/\u03b2 during LCMV infection in vivo. Instead, autocrine amplification through the IFN-\u03b1\/\u03b2R is necessary for optimal induction. In the absence of a functional IFN-\u03b1\/\u03b2R, however, alternative mechanisms, independent of STAT1 but requiring a functional IFN-\u03b3R, take over.<\/jats:p>","DOI":"10.1128\/jvi.76.9.4520-4525.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T09:59:40Z","timestamp":1027763980000},"page":"4520-4525","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":43,"title":["Promotion of Alpha\/Beta Interferon Induction during In Vivo Viral Infection through Alpha\/Beta Interferon Receptor\/STAT1 System-Dependent and -Independent Pathways"],"prefix":"10.1128","volume":"76","author":[{"given":"Lene","family":"Malmgaard","sequence":"first","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thais P.","family":"Salazar-Mather","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Casey A.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christine A.","family":"Biron","sequence":"additional","affiliation":[{"name":"Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.44.29210"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M101216200"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1006\/smim.1998.0138"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(01)00154-6"},{"key":"e_1_3_2_6_2","first-page":"321","year":"2001","unstructured":"Biron, C. 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