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

DOI Web Site 1 Citations
  • Suzanne Fuld
    Lab21 Limited, Unit 184, The Science Park, Cambridge, CB4 0GA, United Kingdom
  • Charles Cunningham
    MRC Virology Unit, Church Street, Glasgow G11 5JR, United Kingdom
  • Kevin Klucher
    Department of Cytokine Biology, ZymoGenetics, Inc., 1201 Eastlake Ave. E., Seattle, Washington 98102
  • Andrew J. Davison
    MRC Virology Unit, Church Street, Glasgow G11 5JR, United Kingdom
  • David J. Blackbourn
    Cancer Research UK Institute for Cancer Studies, University of Birmingham, Birmingham B15 2TT, United Kingdom

Abstract

<jats:title>ABSTRACT</jats:title> <jats:p>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-α/β) signaling. We now show that full-length vIRF-2 protein, translated from two spliced exons, inhibited both IFN-α- and IFN-λ-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-β 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.</jats:p>

Journal

  • Journal of Virology

    Journal of Virology 80 (6), 3092-3097, 2006-03-15

    American Society for Microbiology

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