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

Jun Xu, Leo Luznik, Flossie Wong-Staal, Gordon N. Gill

Research output: Contribution to journalArticlepeer-review

Abstract

Both host cell and viral transcription factors regulate the long terminal repeat (LTR) of human immuno-deficiency virus (HTV) 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.

Original languageEnglish (US)
Pages (from-to)323-331
Number of pages9
JournalJournal of biomedical science
Volume3
Issue number5
DOIs
StatePublished - 1996
Externally publishedYes

Keywords

  • HIV LTR
  • Retinoid receptor
  • Sp1
  • Thyroid hormone receptor
  • Transcription

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Pharmacology (medical)

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