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(Received for publication, May 2, 1996, and in revised form, June 12, 1996)
From the Unité 338 INSERM, 5, rue Blaise Pascal, 67084 Strasbourg Cedex, France
Infection of cells of the central nervous system
by the human immunodeficiency virus type-1 (HIV-1) leads to
HIV-1-associated neuropathology. Recent studies have demonstrated the
importance of long terminal repeat (LTR) binding sites in determining
the pathogenicity of HIV. Here we have investigated the presence and
the functional role of transcription factors that have the potential to
interact, directly or indirectly, with the nuclear receptor-responsive
element in the LTR of HIV-1, in different human cell lines of the
brain. Cotransfection experiments showed that in oligodendroglioma
TC-620 cells, the retinoic acid receptor and the retinoid X receptor
activate LTR-driven transcription in the absence of ligand. Addition of
all-trans- or 9-cis-retinoic acid reverses this
effect. In contrast, in astrocytoma, neuronal, and microglial cells, no
significant effect of the retinoid acid pathway was detected. This
retinoid response is mediated by distinct molecular interactions in the
lymphotropic LAI and the neurotropic JR-CSF HIV-1 strains. Moreover,
retinoid receptors were found to antagonize the chicken ovalbumin
upstream promoter transcription factor- as well as the c-JUN-mediated
LTR transactivation. Our findings demonstrate the importance of the
retinoic acid signaling pathway and of cross-coupling interactions in
the repression of HIV-1 LTR gene expression.
Volume 271, Number 37,
Issue of September 13, 1996
pp. 22895-22900
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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