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Here we demonstrate that gamma interferon (IFN-\u03b3) but not IFN-\u03b1 or IFN-\u03b2 pretreatment of mouse fibroblasts prior to VACV infection induces a long-lasting antiviral state blocking VACV replication. In contrast, high doses of IFN-\u03b3 failed to establish an antiviral state in human fibroblasts. In mouse fibroblasts, IFN-\u03b3 impeded the viral replication cycle at the level of late gene transcription and blocked the multiplication of VACV genomes. The IFN-\u03b3-induced antiviral state invariably prevented the growth of different VACV strains but was not effective against the replication of ectromelia virus. The IFN-\u03b3 effect required intact IFN-\u03b3 receptor signaling prior to VACV infection through Janus kinase 2 (Jak2) and signal transducer and activator of transcription 1 (STAT1). The permissive state of IFN-\u03b3-treated human cells was unrelated to the VACV-encoded IFN decoy receptors B8 and B18 and associated with a complete disruption of STAT1 homodimer formation and DNA binding. Unlike human fibroblasts, mouse cells responded with long-lasting STAT1 activation which was preserved after VACV infection. The deletion of the IFN regulatory factor 1 (IRF-1) gene from mouse cells rescued efficient VACV replication, demonstrating that IRF-1 target genes have a critical role in VACV control. These data have implications for the understanding of VACV pathogenesis and identify an incongruent IFN-\u03b3 response between the human host and the mouse model.<\/jats:p>","DOI":"10.1128\/jvi.02042-08","type":"journal-article","created":{"date-parts":[[2009,2,12]],"date-time":"2009-02-12T05:00:28Z","timestamp":1234414828000},"page":"3684-3695","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["Gamma Interferon-Induced Interferon Regulatory Factor 1-Dependent Antiviral Response Inhibits Vaccinia Virus Replication in Mouse but Not Human Fibroblasts"],"prefix":"10.1128","volume":"83","author":[{"given":"Mirko","family":"Trilling","sequence":"first","affiliation":[{"name":"Institute for Virology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vu Thuy Khanh","family":"Le","sequence":"additional","affiliation":[{"name":"Institute for Virology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert","family":"Zimmermann","sequence":"additional","affiliation":[{"name":"Institute for Virology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holger","family":"Ludwig","sequence":"additional","affiliation":[{"name":"Department of Virology, Paul-Ehrlich-Institut, Langen, D-63225 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus","family":"Pfeffer","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University, Du\u0308sseldorf, D-40225 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerd","family":"Sutter","sequence":"additional","affiliation":[{"name":"Department of Virology, Paul-Ehrlich-Institut, Langen, D-63225 Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geoffrey L.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hartmut","family":"Hengel","sequence":"additional","affiliation":[{"name":"Institute for Virology"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/13.7.897"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.69.8.4633-4639.1995"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.160027697"},{"key":"e_1_3_2_5_2","first-page":"19.7.1","year":"1999","unstructured":"Brune, W., H. 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