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Journal of Virology, April 1999, p. 2694-2702, Vol. 73, No. 4
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Ikappa B-Mediated Inhibition of Virus-Induced Beta Interferon Transcription

Michèle Algarté,1,2 Hannah Nguyen,1,3 Christophe Heylbroeck,1,3 Rongtuan Lin,1,2 and John Hiscott1,2,3,*

Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital,1 and Departments of Microbiology3 and Medicine,2 McGill University, Montreal, Quebec, Canada H3T 1E2

Received 2 September 1998/Accepted 10 December 1998

We have examined the consequences of overexpression of the Ikappa Balpha and Ikappa Bbeta inhibitory proteins on the regulation of NF-kappa B-dependent beta interferon (IFN-beta ) gene transcription in human cells after Sendai virus infection. In transient coexpression studies or in cell lines engineered to express different forms of Ikappa B under tetracycline-inducible control, the IFN-beta promoter (-281 to +19) linked to the chloramphenicol acetyltransferase reporter gene was differentially inhibited in response to virus infection. Ikappa Balpha exhibited a strong inhibitory effect on virus-induced IFN-beta expression, whereas Ikappa Bbeta exerted an inhibitory effect only at a high concentration. Despite activation of the Ikappa B kinase complex by Sendai virus infection, overexpression of the double-point-mutated (S32A/S36A) dominant repressors of Ikappa Balpha (TD-Ikappa Balpha ) completely blocked IFN-beta gene activation by Sendai virus. Endogenous IFN-beta RNA production was also inhibited in Tet-inducible TD-Ikappa Balpha -expressing cells. Inhibition of IFN-beta expression directly correlated with a reduction in the binding of NF-kappa B (p50-RelA) complex to PRDII after Sendai virus infection in Ikappa Balpha -expressing cells, whereas IFN-beta expression and NF-kappa B binding were only slightly reduced in Ikappa Bbeta -expressing cells. These experiments demonstrate a major role for Ikappa Balpha in the regulation of NF-kappa B-induced IFN-beta gene activation and a minor role for Ikappa Bbeta in the activation process.

* Corresponding author. Mailing address: Lady Davis Institute for Medical Research, 3755 Cote Ste. Catherine, Montreal, Quebec, Canada H3T1E2. Phone: (514) 340-8222, ext. 5265. Fax: (514) 340-7576. E-mail: mijh{at}musica.mcgill.ca.

Journal of Virology, April 1999, p. 2694-2702, Vol. 73, No. 4
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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