This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Strähle, L.
Right arrow Articles by Garcin, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Strähle, L.
Right arrow Articles by Garcin, D.

 Previous Article  |  Next Article 

Journal of Virology, November 2007, p. 12227-12237, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01300-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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

Laura Strähle, Jean-Baptiste Marq, Albert Brini, Stéphane Hausmann, Daniel Kolakofsky,* and Dominique Garcin

Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland

Received 14 June 2007/ Accepted 27 August 2007

As infection with wild-type (wt) Sendai virus (SeV) normally activates beta interferon (IFN-ß) very poorly, two unnatural SeV infections were used to study virus-induced IFN-ß 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-ß 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-ß. Nondefective SeV that cannot specifically express C proteins not only cannot prevent the effects of transfected poly(I-C) or pppRNAs on IFN-ß 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.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Medicine, University of Geneva School of Medicine, 11 Ave. de Champel, CH1211 Geneva, Switzerland. Phone: 41-223795657. Fax: 41-223795702. E-mail: Daniel.Kolakofsky{at}medecine.unige.ch

{triangledown} Published ahead of print on 5 September 2007.

Journal of Virology, November 2007, p. 12227-12237, Vol. 81, No. 22
0022-538X/07/$08.00+0     doi:10.1128/JVI.01300-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Drahos, J., Racaniello, V. R. (2009). Cleavage of IPS-1 in Cells Infected with Human Rhinovirus. J. Virol. 83: 11581-11587 [Abstract] [Full Text]  
  • Marq, J.-B., Hausmann, S., Luban, J., Kolakofsky, D., Garcin, D. (2009). The Double-stranded RNA Binding Domain of the Vaccinia Virus E3L Protein Inhibits Both RNA- and DNA-induced Activation of Interferon {beta}. J. Biol. Chem. 284: 25471-25478 [Abstract] [Full Text]  
  • Manuse, M. J., Parks, G. D. (2009). Role for the Paramyxovirus Genomic Promoter in Limiting Host Cell Antiviral Responses and Cell Killing. J. Virol. 83: 9057-9067 [Abstract] [Full Text]  
  • Chambers, R., Takimoto, T. (2009). Host specificity of the anti-interferon and anti-apoptosis activities of parainfluenza virus P/C gene products. J. Gen. Virol. 90: 1906-1915 [Abstract] [Full Text]  
  • Parisien, J.-P., Bamming, D., Komuro, A., Ramachandran, A., Rodriguez, J. J., Barber, G., Wojahn, R. D., Horvath, C. M. (2009). A Shared Interface Mediates Paramyxovirus Interference with Antiviral RNA Helicases MDA5 and LGP2. J. Virol. 83: 7252-7260 [Abstract] [Full Text]  
  • Childs, K. S., Andrejeva, J., Randall, R. E., Goodbourn, S. (2009). Mechanism of mda-5 Inhibition by Paramyxovirus V Proteins. J. Virol. 83: 1465-1473 [Abstract] [Full Text]  
  • Deng, L., Dai, P., Parikh, T., Cao, H., Bhoj, V., Sun, Q., Chen, Z., Merghoub, T., Houghton, A., Shuman, S. (2008). Vaccinia Virus Subverts a Mitochondrial Antiviral Signaling Protein-Dependent Innate Immune Response in Keratinocytes through Its Double-Stranded RNA Binding Protein, E3. J. Virol. 82: 10735-10746 [Abstract] [Full Text]  
  • Bitko, V., Musiyenko, A., Bayfield, M. A., Maraia, R. J., Barik, S. (2008). Cellular La Protein Shields Nonsegmented Negative-Strand RNA Viral Leader RNA from RIG-I and Enhances Virus Growth by Diverse Mechanisms. J. Virol. 82: 7977-7987 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»