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Journal of Virology, March 2006, p. 3092-3097, Vol. 80, No. 6
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.6.3092-3097.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Inhibition of Interferon Signaling by the Kaposi's Sarcoma-Associated Herpesvirus Full-Length Viral Interferon Regulatory Factor 2 Protein

Lab21 Limited, Unit 184, The Science Park, Cambridge, CB4 0GA, United Kingdom,¹ MRC Virology Unit, Church Street, Glasgow G11 5JR, United Kingdom,² Department of Cytokine Biology, ZymoGenetics, Inc., 1201 Eastlake Ave. E., Seattle, Washington 98102,³ Cancer Research UK Institute for Cancer Studies, University of Birmingham, Birmingham B15 2TT, United Kingdom⁴

Received 18 April 2005/ Accepted 28 December 2005

Interferon (IFN) signal transduction involves interferon regulatory factors (IRF). Kaposi's sarcoma-associated herpesvirus (KSHV) encodes four IRF homologues: viral IRF 1 (vIRF-1) to vIRF-4. Previous functional studies revealed that the first exon of vIRF-2 inhibited alpha/beta interferon (IFN-/ß) signaling. We now show that full-length vIRF-2 protein, translated from two spliced exons, inhibited both IFN-- and IFN--driven transactivation of a reporter promoter containing the interferon stimulated response element (ISRE). Transactivation of the ISRE promoter by IRF-1 was negatively regulated by vIRF-2 protein as well. Transactivation of a full-length IFN-ß reporter promoter by either IRF-3 or IRF-1, but not IRF-7, was also inhibited by vIRF-2 protein. Thus, vIRF-2 protein is an interferon induction antagonist that acts pleiotropically, presumably facilitating KSHV infection and dissemination in vivo.

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