Dioxin activates human immunodeficiency virus-1 expression in chronically infected promonocytic U1 cells by enhancing NF-kappa B activity and production of tumor necrosis factor-alpha

Biochem Biophys Res Commun. 1996 Sep 24;226(3):889-94. doi: 10.1006/bbrc.1996.1445.


Dioxin, a prevalent environmental pollutant, is known to enhance replication of viruses in animals, but the mechanism is poorly understood. Here we report that dioxin triggers human immunodeficiency virus-1 (HIV-1) gene expression, resulting in increased production of HIV in chronically infected promonocytic U1 cells. This effect of dioxin is mediated, in part, via activation of nuclear factor kappa-B (NF-kappa B), a key cellular transcription factor that plays an important role in the induction of HIV genes and cytokine genes that regulate HIV-replication. Dioxin stimulated the production of tumor necrosis-alpha in U1 cells, and pentoxifylline, an inhibitor of TNF-alpha synthesis, inhibited dioxin induced HIV production and TNF-alpha. These studies provide a molecular and cellular basis for increased viral replication in cells exposed to dioxin.

MeSH terms

  • Base Sequence
  • Binding Sites
  • Cell Survival / drug effects
  • Dioxins / pharmacology*
  • Gene Expression / drug effects
  • Genes, Viral
  • HIV Core Protein p24 / analysis
  • HIV Core Protein p24 / biosynthesis
  • HIV-1 / drug effects
  • HIV-1 / physiology*
  • Humans
  • NF-kappa B / metabolism*
  • Oligonucleotide Probes
  • Pentoxifylline / pharmacology
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Virus Replication / drug effects*


  • Dioxins
  • HIV Core Protein p24
  • NF-kappa B
  • Oligonucleotide Probes
  • Tumor Necrosis Factor-alpha
  • Pentoxifylline