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Journal of Virology, November 2007, p. 12005-12018, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.01359-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Differential Expression of Interferon (IFN) Regulatory Factors and IFN-Stimulated Genes at Early Times after West Nile Virus Infection of Mouse Embryo Fibroblasts{triangledown}

Svetlana V. Scherbik, Bronislava M. Stockman, and Margo A. Brinton*

Department of Biology, Georgia State University, Atlanta, Georgia 30302

Received 21 June 2007/ Accepted 16 August 2007

Although lineage I West Nile virus (WNV) strain Eg101 induced beta interferon (IFN-ß) production as early as 12 h after infection in primary mouse embryo fibroblasts and did not inhibit the JAK-STAT signaling pathway, it was still able to replicate efficiently. To gain insights about possible viral countermeasures used by this virus to suppress the host response, the cell transcriptional profile and the kinetics of IFN regulatory factor (IRF) expression and activation were examined at early times after infection. By 12 h after WNV infection, the majority of the up-regulated genes were ones involved in IFN pathways. However, comparison of IFN-stimulated gene (ISG) expression levels in mock-infected, IFN-treated, and virus-infected cells indicated that WNV infection suppressed the up-regulation of a subset of ISGs, including genes involved in transcriptional regulation, apoptosis, and stress responses, prior to 24 h after infection. Analysis of mRNA and protein levels for representative genes indicated that suppression was at the transcriptional and posttranscriptional levels. Translocation of IRF-3 to the nucleus was observed beginning at 8 h, IRF-7 expression was detected by 12 h, but IRF-1 expression was not detected until 24 h after infection. Virus-induced gene suppression was sufficient to overcome the effect of exogenous IFN pretreatment for 1 h but not for 4 h prior to infection. These data indicate that WNV can selectively counteract the host response at early times after infection by previously unreported mechanisms.

* Corresponding author. Mailing address: Department of Biology, Georgia State University, P.O. Box 4010, Atlanta, GA 30302-4010. Phone: (404) 413-5388. Fax: (404) 413-5301. E-mail: mbrinton{at}gsu.edu

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

Journal of Virology, November 2007, p. 12005-12018, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.01359-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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