The Journal of Experimental Medicine
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Published 20 May 2002. doi:10.1084/jem.20010753
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© Rockefeller University Press, 0022-1007/2002/5/1359/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 10, May 20, 2002 1359-1370

Modulation of Human Immunodeficiency Virus 1 Replication by Interferon Regulatory Factors

Marco Sgarbanti1, Alessandra Borsetti1, Nicola Moscufo2, Maria C. Bellocchi1, Barbara Ridolfi1, Filomena Nappi1, Giulia Marsili1, Giovanna Marziali1, Eliana M. Coccia3, Barbara Ensoli1 and Angela Battistini1

1 Laboratory of Virology, Istituto Superiore di Sanità, 00161 Rome, Italy
2 Laboratory of Cellular Biology, Istituto Superiore di Sanità, 00161 Rome, Italy
3 Laboratory of Immunology, Istituto Superiore di Sanità, 00161 Rome, Italy

Address correspondence to A. Battistini, Laboratory of Virology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Phone: 39-06-49903266; Fax: 39-06-49902082; E-mail: battist{at}iss.it or to Dr. B. Ensoli, Laboratory of Virology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy. Phone: 39-06-49903208; Fax: 39-06-49903002; E-mail: ensoli{at}iss.it

Transcription of the human immunodeficiency virus (HIV)-1 is controlled by the cooperation of virally encoded and host regulatory proteins. The Tat protein is essential for viral replication, however, expression of Tat after virus entry requires HIV-1 promoter activation. A sequence in the 5' HIV-1 LTR, containing a binding site for transcription factors of the interferon regulatory factors (IRF) family has been suggested to be critical for HIV-1 transcription and replication. Here we show that IRF-1 activates HIV-1 LTR transcription in a dose-dependent fashion and in the absence of Tat. This has biological significance since IRF-1 is produced early upon virus entry, both in cell lines and in primary CD4+ T cells, and before expression of Tat. IRF-1 also cooperates with Tat in amplifying virus gene transcription and replication. This cooperation depends upon a physical interaction that is blocked by overexpression of IRF-8, the natural repressor of IRF-1, and, in turn is released by overexpression of IRF-1. These data suggest a key role of IRF-1 in the early phase of viral replication and/or during viral reactivation from latency, when viral transactivators are absent or present at very low levels, and suggest that the interplay between IRF-1 and IRF-8 may play a key role in virus latency.

Key Words: virus replication • Tat • transcription factors • gene expression • T lymphocytes


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