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Published ahead of print on October 19, 2006, doi:10.1165/rcmb.2006-0283RC

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 3, March 2007, 263-269

A more recent version of this article appeared on March 1, 2007
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Submitted on August 3, 2006
Revised on October 19, 2006

NS1 Protein of Influenza A Virus Inhibits the Function of Intracytoplasmic Pathogen Sensor, RIG-I

Zhu Guo1, Li-mei Chen1, Hui Zeng1, Jorge A Gomez1, Julie Plowden1, Takashi Fujita2, Jacqueline M Katz1, Ruben O Donis1, and Suryaprakash Sambhara1*

1 Influenza Division, Centers for Disease Control and Prevention, Atlanta, GA, USA, 2 Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto, Japan

* To whom correspondence should be addressed. E-mail: ssambhara{at}cdc.gov.

Retinoic acid-inducible gene I (RIG-I) has recently been identified as one of the key intracellular sensors of virus infection. RIG-I binds to cytosolic double-stranded RNA and initiates a signaling cascade that leads to the activation of transcription factors required for expression of type I interferon (IFN-I). Previous evidence suggests that nonstructural protein 1 (NS1) encoded by influenza A virus (IAV) suppresses IFN-I secretion in virus-infected cells by an unknown mechanism. In the present study, we demonstrate that RIG-I is required for induction of IFN-I in an IAV-infected human lung epithelial cell line. Knockdown of RIG-I expression by RNA interference greatly impairs production of interferon beta in cells infected with different strains of wild type IAV. Furthermore, co-expression of IAV NS1 downregulates production of IFN {beta} induced by RIG-I agonists, and ectopic expression of RIG-I inhibits the replication of IAV. These results provide further information on the mechanism by which IAV NS1 antagonizes the host antiviral response.




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