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Journal of Virology, December 2000, p. 11566-11573, Vol. 74, No. 24
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Influenza A Virus NS1 Protein Prevents Activation of NF-kappa B and Induction of Alpha/Beta Interferon

Xiuyan Wang,1 Ming Li,2 Hongyong Zheng,1 Thomas Muster,3 Peter Palese,1 Amer A. Beg,2 and Adolfo García-Sastre1,*

Department of Microbiology, Mount Sinai School of Medicine, New York, New York 10029,1 Department of Biological Sciences, Columbia University, New York, New York 10027,2 and Department of Dermatology, University of Vienna Medical School, 1090 Vienna, Austria3

Received 28 July 2000/Accepted 11 September 2000

The alpha/beta interferon (IFN-alpha /beta ) system represents one of the first lines of defense against virus infections. As a result, most viruses encode IFN antagonistic factors which enhance viral replication in their hosts. We have previously shown that a recombinant influenza A virus lacking the NS1 gene (delNS1) only replicates efficiently in IFN-alpha /beta -deficient systems. Consistent with this observation, we found that infection of tissue culture cells with delNS1 virus, but not with wild-type influenza A virus, induced high levels of mRNA synthesis from IFN-alpha /beta genes, including IFN-beta . It is known that transactivation of the IFN-beta promoter depends on NF-kappa B and several other transcription factors. Interestingly, cells infected with delNS1 virus showed high levels of NF-kappa B activation compared with those infected with wild-type virus. Expression of dominant-negative inhibitors of the NF-kappa B pathway during delNS1 virus infection prevented the transactivation of the IFN-beta promoter, demonstrating a functional link between NF-kappa B activation and IFN-alpha /beta synthesis in delNS1 virus-infected cells. Moreover, expression of the NS1 protein prevented virus- and/or double-stranded RNA (dsRNA)-mediated activation of the NF-kappa B pathway and of IFN-beta synthesis. This inhibitory property of the NS1 protein of influenza A virus was dependent on its ability to bind dsRNA, supporting a model in which binding of NS1 to dsRNA generated during influenza virus infection prevents the activation of the IFN system. NS1-mediated inhibition of the NF-kappa B pathway may thus play a key role in the pathogenesis of influenza A virus.

* Corresponding author. Mailing address: Department of Microbiology, Mount Sinai School of Medicine, Box 1124, One Gustave L. Levy Place, New York, NY 10029. Phone: (212) 241-7769. Fax: (212) 534-1684. E-mail: adolfo.garcia-sastre{at}mssm.edu.

Journal of Virology, December 2000, p. 11566-11573, Vol. 74, No. 24
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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