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J Virol, July 1998, p. 5862-5869, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Retinoid-Induced Repression of Human Immunodeficiency Virus Type 1 Core Promoter Activity Inhibits Virus Replication

Joseph W. Maciaszek,1 Salvatore J. Coniglio,2 David A. Talmage,3 and Gregory A. Viglianti2,*

Program in Virology and Immunology, University of Massachusetts Medical Center, Worcester, Massachusetts 016051; Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts 021182; and Institute of Human Nutrition, Columbia University, New York, New York 100323

Received 16 January 1998/Accepted 15 April 1998

The rates of mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1), progression to AIDS following HIV-1 infection, and AIDS-associated mortality are all inversely correlated with serum vitamin A levels (R. D. Semba, W. T. Caiaffa, N. M. H. Graham, S. Cohn, and D. Vlahov, J. Infect. Dis. 171:1196-1202, 1995; R. D. Semba, N. M. H. Graham, W. T. Caiaffa, J. B. Margolik, L. Clement, and D. Vlahov, Arch. Intern. Med. 153:2149-2154, 1993; R. D. Semba, P. G. Miotti, J. D. Chiphangwi, A. J. Saah, J. K. Canner, G. A. Dallabetta, and D. R. Hoover, Lancet 343:1593-1596, 1994). Here we show that physiological concentrations of vitamin A, as retinol or as its metabolite, all-trans retinoic acid, repressed HIV-1Ba-L replication in monocyte-derived macrophages (MDMs). Repression required retinoid treatment of peripheral monocytes during their in vitro differentiation into MDMs. Retinoids had no repressive effect if they were added after virus infection. Retinol, as well as all-trans retinoic acid and 9-cis retinoic acid, also repressed HIV-1 long terminal repeat (LTR)-directed expression up to 200-fold in transfected THP-1 monocytes. Analysis of HIV-1 LTR deletion mutants demonstrated that retinoids were able to repress activation of HIV-1 expression by both NF-kappa B and Tat. A cis-acting sequence required for retinoid-mediated repression of HIV-1 transcription was localized between nucleotides -51 and +12 of the HIV-1 LTR within the core promoter. Protein-DNA cross-linking experiments identified four proteins specific to retinoid-treated cells that bound to the core promoter. We conclude that retinoids render macrophages resistant to virus replication by modulating the interaction of cellular transcription factors with the viral core promoter.

* Corresponding author. Mailing address: Department of Microbiology, Boston University School of Medicine, 715 Albany St., Boston, MA 02118. Phone: (617) 638-7790. Fax: (617) 638-4286. E-mail: gviglian{at}bu.edu.

J Virol, July 1998, p. 5862-5869, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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