Hormone Receptor Regulation of the Human Immunodeficiency Virus Type 1 and Type 2 Long Terminal Repeats.
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 (T(3)R 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 T(3)R 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 approximately 5-fold by ligand-activated T(3)R, approximately 10-fold by ligand-activated RXR and 20- to 30-fold by both receptors and their cognate ligands. T(3)R.RXR heterodimers bound to NF-kappaB and Sp1 response elements in both HIV LTRs having highest affinity for the HIV-1 NF-kappaB region. When U937 monocytic cells were cotransfected with HIV-1 viral DNA and T(3)R, 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. Copyright 1996 S. Karger AG, Basel
Xu
J.
J
Department of Biology, University of California San Diego, La Jolla, Calif., USA.
Luznik
L.
L
Wong-Staal
F.
F
Gill
G.N.
GN