- 作者: Jun Xu; Leo Luznik; Flossie Wong-Staal; Gordon N. Gill
- 作者服務機構: Departments of ; a Biology and; b Medicine, University of California San Diego, La Jolla, Calif, USA
- 中文摘要: --
- 英文摘要: 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. Drosoph-ila SL2 cells that lack Spl 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 Spl 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.
- 中文關鍵字: --
- 英文關鍵字: Thyroid hormone receptor; Retinoid receptor; HIV LTR; Transcription; Sp1