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Journal of Virology, April 2005, p. 3920-3929, Vol. 79, No. 7
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.7.3920-3929.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Analysis of Genes Induced by Sendai Virus Infection of Mutant Cell Lines Reveals Essential Roles of Interferon Regulatory Factor 3, NF-{kappa}B, and Interferon but Not Toll-Like Receptor 3{dagger}

Christopher P. Elco,1,2 Jeanna M. Guenther,3 Bryan R. G. Williams,2,3 and Ganes C. Sen1,2*

Departments of Molecular Biology,1 Cancer Biology, Lerner Research Institute, The Cleveland Clinic Foundation,3 Graduate Program in Molecular Virology, Case Western Reserve University, Cleveland, Ohio2

Received 9 September 2004/ Accepted 12 November 2004

Sendai virus (SeV) infection causes the transcriptional induction of many cellular genes that are also induced by interferon (IFN) or double-stranded RNA (dsRNA). We took advantage of various mutant cell lines to investigate the putative roles of the components of the IFN and dsRNA signaling pathways in the induction of those genes by SeV. Profiling the patterns of gene expression in SeV-infected cells demonstrated that Toll-like receptor 3, although essential for gene induction by dsRNA, was dispensable for gene induction by SeV. In contrast, Jak1, which mediates IFN signaling, was required for the induction of a small subset of genes by SeV. NF-{kappa}B and interferon regulatory factor 3 (IRF-3), the two major transcription factors activated by virus infection, were essential for the induction of two sets of genes by SeV. As expected, some of the IRF-3-dependent genes, such as ISG56, were more strongly induced by SeV in IRF-3-overexpressing cells. Surprisingly, in those cells, a number of NF-{kappa}B-dependent genes, such as the A20 gene, were induced poorly. Using a series of cell lines expressing increasing levels of IRF-3, we demonstrated that the degree of induction of A20 mRNA, upon SeV infection, was inversely proportional to the cellular level of IRF-3, whereas that of ISG56 mRNA was directly proportional. Thus, IRF-3 can suppress the expression of NF-{kappa}B-dependent genes in SeV-infected cells.

* Corresponding author. Mailing address: Dept. of Molecular Biology/NC20, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195. Phone: (216) 444-0636. Fax: (216) 444-0513. E-mail: seng{at}ccf.org.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, April 2005, p. 3920-3929, Vol. 79, No. 7
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.7.3920-3929.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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