Hormone receptor regulation of the human immunodeficiency virus type 1 and type 2 long terminal repeats

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Abstract
Both host cell and viral transcription factors regulate the long terminal repeat (LTR) of human immuno-deficiency virus (HIV) activity and viral replication. Using transient transfection, ligand-activated thyroid hormone and 9-cis-retinoic acid receptors (T3R and RXR) were found to stimulate HIV-1 and HIV-2 LTR activities. They also stimulated HIV-1 viral production. Drosophila SL2 cells that lack Sp1 and T3R were used to study HIV-1 and HIV-2 LTR activities. Both activities were stimulated by cotransfection of SP1 (120- and 180-fold, respectively); HIV LTR activities were also stimulated ∼ 5-fold by ligand-activated T3R, ∼ 10-fold by ligand-activated RXR and 20- to 30-fold by both receptors and their cognate ligands. T3R·RXR heterodimers bound to NF-κB and Sp1 response elements in both HIV LTRs having highest affinity for the HIV-1 NF-κB region. When U937 monocytic cells were cotransfected with HIV-1 viral DNA and T3R, RXR and retinoic acid receptor (RAR) expression plasmids, hormonal treatment increased viral replication up to 5-fold. Hormonal signals thus have the potential to regulate HIV transcription and viral production.