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Journal of Virology, August 1999, p. 7080-7086, Vol. 73, No. 8
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Human Immunodeficiency Virus Type 1 Tat Protein Activates Transcription Factor NF-kappa B through the Cellular Interferon-Inducible, Double-Stranded RNA-Dependent Protein Kinase, PKR

Francesca Demarchi,1 Maria Ines Gutierrez,1 and Mauro Giacca1,2,*

Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology, 34012 Trieste,1 and Istituto di Genetica Biochimica ed Evoluzionistica del CNR, 27100 Pavia,2 Italy

Received 19 January 1999/Accepted 7 May 1999

The transactivator protein of human immunodeficiency virus type 1 (HIV-1) (Tat) is a powerful activator of nuclear factor-kappa B (NF-kappa B), acting through degradation of the inhibitor Ikappa B-alpha (F. Demarchi, F. d'Adda di Fagagna, A. Falaschi, and M. Giacca, J. Virol. 70:4427-4437, 1996). Here, we show that this activity of Tat requires the function of the cellular interferon-inducible protein kinase PKR. Tat-mediated NF-kappa B activation and transcriptional induction of the HIV-1 long terminal repeat were impaired in murine cells in which the PKR gene was knocked out. Both functions were restored by cotransfection of Tat with the cDNA for PKR. Expression of a dominant-negative mutant of PKR specifically reduced the levels of Tat transactivation in different human cell types. Activation of NF-kappa B by Tat required integrity of the basic domain of Tat; previous studies have indicated that this domain is necessary for specific Tat-PKR interaction.

* Corresponding author. Mailing address: Molecular Medicine Laboratory, ICGEB, Padriciano, 99, 34012 Trieste, Italy. Phone: 390-40-3757.324. Fax: 390-40-226555. E-mail: giacca{at}icgeb.trieste.it.

Journal of Virology, August 1999, p. 7080-7086, Vol. 73, No. 8
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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