Stimulation of the Human Immunodeficiency Virus Type-1 Enhancer by the Human T-Cell Leukemia-Virus Type-I Tax Gene-Product Involves the Action of Inducible Cellular Proteins

Bohnlein, E., Siekevitz, M., Ballard, D. W., Lowenthal, J. W., Rimsky, L., Bogerd, H., Hoffman, J., Wano, Y., Franza, B. R., Greene, W. C. (April 1989) Stimulation of the Human Immunodeficiency Virus Type-1 Enhancer by the Human T-Cell Leukemia-Virus Type-I Tax Gene-Product Involves the Action of Inducible Cellular Proteins. Journal of Virology, 63 (4). pp. 1578-1586. ISSN 0022-538X

URL: http://www.ncbi.nlm.nih.gov/pubmed/2784507

Abstract

The human immunodeficiency virus type 1 (HIV-1) preferentially infects CD4+ T lymphocytes and may exist as a latent provirus within these cells for extended periods. The transition to a productive retroviral infection results in T-cell death and clinically may lead to the acquired immune deficiency syndrome. Accelerated production of infectious HIV-1 virions appears to be closely linked to a heightened state of T-cell activation. The transactivator (Tax) protein of the type I human T-cell leukemia virus (HTLV-I) can produce such an activated T-cell phenotype and augments activity of the HIV-1 long terminal repeat. One Tax-responsive region within the HIV-1 long terminal repeat has been mapped to a locus composed of two 10-base-pair direct repeats sharing homology with the binding site for the eucaryotic transcription factor NF-kappaB (GGGACTTTCC). Tax-expressing Jurkat T cells contain one or more inducible cellular proteins that specifically associate with the HIV-1 enhancer at these binding sites. Microscale DNA affinity precipitation assays identified a Tax-inducible 86-kilodalton protein, HIVEN86A, as one of these HIV-1 enhancer-binding factors. The interaction of HIVEN86A, and presumably other cellular proteins, with the HIV-1 enhancer appears functionally important as oligonucleotides corresponding to this enhancer were sufficient to impart Tax inducibility to an unresponsive heterologous promoter. These findings suggest that the Tax-inducible cellular protein HIVEN86A plays an important role in the transcriptional activation of the HIV-1 enhancer. These specific protein-DNA interactions may also be important for the transition of HIV-1 from a latent to a productive mode of infection. Furthermore, these findings highlight an intriguing biological interplay between HTLV-1 and HIV-1 through a cellular transcriptional pathway that is normally involved in T-cell activation and growth.

Item Type: Paper
Subjects: organs, tissues, organelles, cell types and functions > cell types and functions > cell types > T cells
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > T cells
organs, tissues, organelles, cell types and functions > cell types and functions > cell types > T cells

organism description > animal > mammal > primates > hominids > human
diseases & disorders > cancer > cancer types > leukemia
CSHL Authors:
Communities: CSHL labs
Depositing User: Gail Sherman
Date: April 1989
Date Deposited: 02 Aug 2017 14:39
Last Modified: 02 Aug 2017 14:39
PMCID: PMC248395
Related URLs:
URI: http://repository.cshl.edu/id/eprint/34831

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