Rabies Virus P Protein Interacts with STAT1 and Inhibits Interferon Signal Transduction Pathways

DOI Web Site 被引用文献15件
  • Aurore Vidy
    Unité Mixte de Virologie Moléculaire et Structurale UMR 2472 CNRS, UMR1157 INRA, 91198 Gif sur Yvette Cedex, France
  • Mounira Chelbi-Alix
    UPR 9045 CNRS, Institut Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France
  • Danielle Blondel
    Unité Mixte de Virologie Moléculaire et Structurale UMR 2472 CNRS, UMR1157 INRA, 91198 Gif sur Yvette Cedex, France

抄録

<jats:title>ABSTRACT</jats:title> <jats:p> Rabies virus P protein is a cofactor of RNA polymerase. We investigated other potential roles of P (CVS strain) by searching for cellular partners using two-hybrid screening. We isolated a cDNA encoding the signal transducer and activator of transcription 1 (STAT1) that is a critical component of interferon type I (IFN-α/β) and type II (IFN-γ) signaling. We confirmed this interaction by glutathione <jats:italic>S</jats:italic> -transferase-pull-down assay. Deletion mutant analysis indicated that the carboxy-terminal part of P interacted with a region containing the DNA-binding domain and the coiled-coil domain of STAT1. The expression of P protein inhibits IFN-α- and IFN-γ-induced transcriptional responses, thus impairing the IFN-induced antiviral state. Mechanistic studies indicate that P protein does not induce STAT1 degradation and does not interfere with STAT1 phosphorylation but prevents IFN-induced STAT1 nuclear accumulation. These results indicate that rabies P protein overcomes the antiviral response of the infected cells. </jats:p>

収録刊行物

  • Journal of Virology

    Journal of Virology 79 (22), 14411-14420, 2005-11-15

    American Society for Microbiology

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