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Activation of the Beta Interferon Promoter by Unnatural Sendai Virus Infection Requires RIG-I and Is Inhibited by Viral C Proteins

  • Strähle, Laura Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
  • Marq, Jean-Baptiste Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
  • Brini, Albert Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
  • Hausmann, Stéphane Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
  • Kolakofsky, Daniel Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
  • Garcin, Dominique Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland
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Published in:
  • Journal of Virology. - American Society for Microbiology. - 2007, vol. 81, no. 22, p. 12227-12237
Immunology
Insect Science
Microbiology
Virology
English ABSTRACT
As infection with wild-type (wt) Sendai virus (SeV) normally activates beta interferon (IFN-β) very poorly, two unnatural SeV infections were used to study virus-induced IFN-β activation in mouse embryonic fibroblasts: (i) SeV-DI-H4, which is composed mostly of small, copyback defective interfering (DI) genomes and whose infection overproduces short 5′-triphosphorylated trailer RNAs (pppRNAs) and underproduces viral V and C proteins, and (ii) SeV-GFP(+/−), a coinfection that produces wt amounts of viral gene products but that also produces both green fluorescent protein (GFP) mRNA and its complement, which can form double-stranded RNA (dsRNA) with capped 5′ ends. We found that (i) virus-induced signaling to IFN-β depended predominantly on RIG-I (as opposed to mda-5) for both SeV infections, i.e., that RIG-I senses both pppRNAs and dsRNA without 5′-triphosphorylated ends, and (ii) it is the viral C protein (as opposed to V) that is primarily responsible for countering RIG-I-dependent signaling to IFN-β. Nondefective SeV that cannot specifically express C proteins not only cannot prevent the effects of transfected poly(I-C) or pppRNAs on IFN-β activation but also synergistically enhances these effects. SeV-Vminus infection, in contrast, behaves mostly like wt SeV and counteracts the effects of transfected poly(I-C) or pppRNAs.
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  • English
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bronze
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https://sonar.ch/global/documents/249998
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