This Article Full Text (PDF) Other Versions of this Article: JVI.01300-07v1 81/22/12227    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Strähle, L. Articles by Garcin, D. Search for Related Content PubMed PubMed Citation Articles by Strähle, L. Articles by Garcin, D.

 Previous Article  |  Next Article 

J. Virol. doi:10.1128/JVI.01300-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Activation of the IFN promoter by unnatural Sendai virus infection requires RIG-I and is inhibited by the viral C proteins

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

	Abstract

As infection with wild-type Sendai virus normally activates IFN very poorly, two unnatural SeV infections were used to study virus-induced IFN activation in MEFs; 1) SeV-DI-H4, which is composed mostly of small, copyback DI genomes, and whose infection over-produces short 5' tri-phosphorylated (ppp) trailer RNAs and under-produces the viral V and C proteins, and 2) SeV-GFP(+/-), a co-infection that produces wt amounts of viral gene products but also produces both GFP mRNA and its complement, which can form dsRNA with capped 5' ends. We found that 1) virus-induced signaling to IFN 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' tri-phosphorylated ends, and 2) that it is the viral C protein (as opposed to V) that is primarily responsible for countering RIG-I dependent signaling to IFN. Nondefective SeV that cannot specifically express the C proteins not only cannot prevent the effects of transfected poly I/C or _pppRNAs on IFN activation, but rather synergistically enhances these effects. SeV-V^minus infection, in contrast, behaves mostly like SeV-wt, and counteracts the effects of transfected poly I/C or _pppRNAs

This article has been cited by other articles:

• 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]