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Journal of Virology, November 2007, p. 11809-11816, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.00791-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Differential Effects of Mutations in NS4B on West Nile Virus Replication and Inhibition of Interferon Signaling{triangledown}

Jared D. Evans* and Christoph Seeger

Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111

Received 12 April 2007/ Accepted 8 August 2007

West Nile virus (WNV) is a human pathogen that can cause symptomatic infections associated with meningitis and encephalitis. Previously, we demonstrated that replication of WNV inhibits the interferon (IFN) signal transduction pathway by preventing the accumulation of phosphorylated Janus kinase 1 (JAK1) and tyrosine kinase 2 (Tyk2) (J. T. Guo et al., J. Virol. 79:1343-1350, 2005). Through a genetic analysis, we have now identified a determinant on the nonstructural protein 4B (NS4B) that controls IFN resistance in HeLa cells expressing subgenomic WNV replicons lacking the structural genes. However, in the context of infectious genomes, the same determinant did not influence IFN signaling. Thus, our results indicate that NS4B may be sufficient to inhibit the IFN response in replicon cells and suggest a role for structural genes, or as yet unknown interactions, in the inhibition of the IFN signaling pathway during WNV infections.

* Corresponding author. Mailing address: Fox Chase Cancer Center, Institute for Cancer Research, 333 Cottman Ave., Philadelphia, PA 19111. Phone: (215) 728-4313. Fax: (215) 728-3574. E-mail: jared.evans{at}fccc.edu

{triangledown} Published ahead of print on 22 August 2007.

Journal of Virology, November 2007, p. 11809-11816, Vol. 81, No. 21
0022-538X/07/$08.00+0     doi:10.1128/JVI.00791-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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