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Several studies have highlighted the importance of mouse interferons (IFNs) in resistance to and recovery from EV infection, but little is known of the anti-IFN strategies encoded by the virus itself. We have determined that 12 distinct strains and isolates of EV encode soluble, secreted receptors for IFN-\u03b3 (vIFN-\u03b3R) and IFN-\u03b1\/\u03b2 (vIFN-\u03b1\/\u03b2R) that are homologous to those identified in other OPVs. We demonstrate for the first time that the EV vIFN-\u03b3R has the unique ability to inhibit the biological activity of mouse IFN-\u03b3. The EV vIFN-\u03b1\/\u03b2R was a potent inhibitor of human and mouse IFN-\u03b1 and human IFN-\u03b2 but, surprisingly, was unable to inhibit mouse IFN-\u03b2. The replication of all of the EVs included in our study and of cowpox virus was more resistant than VV to the antiviral effects induced in mouse L-929 cells by IFN-\u03b1\/\u03b2 and IFN-\u03b3. Sequencing studies showed that this EV resistance is likely to be partly mediated by the double-stranded-RNA-binding protein encoded by an intact EV homolog of the VV E3L gene. The absence of a functional K3L gene, which encodes a viral eIF-2\u03b1 homolog, in EV suggests that the virus encodes a novel mechanism to counteract the IFN response. These findings will facilitate future studies of the role of viral anti-IFN strategies in mousepox pathogenesis. Their significance in the light of earlier data on the role of IFNs in mousepox is discussed.<\/jats:p>","DOI":"10.1128\/jvi.76.3.1124-1134.2002","type":"journal-article","created":{"date-parts":[[2010,10,27]],"date-time":"2010-10-27T14:32:49Z","timestamp":1288189969000},"page":"1124-1134","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":57,"title":["Inhibition of Interferons by Ectromelia Virus"],"prefix":"10.1128","volume":"76","author":[{"given":"Vincent P.","family":"Smith","sequence":"first","affiliation":[{"name":"Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio","family":"Alcami","sequence":"additional","affiliation":[{"name":"Division of Virology, Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(88)90050-5"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-80-4-949"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0167-5699(00)01699-6"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0147-9571(96)00013-6"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(92)90274-G"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.69.8.4633-4639.1995"},{"key":"e_1_3_2_8_2","doi-asserted-by":"crossref","first-page":"624","DOI":"10.4049\/jimmunol.160.2.624","volume":"160","year":"1998","unstructured":"Alcami, A., J. 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