Tumor necrosis factor alpha activates human immunodeficiency virus type 1 through induction of nuclear factor binding to the NF-kappa B sites in the long terminal repeat

Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8. doi: 10.1073/pnas.86.15.5974.


Expression of human immunodeficiency virus type 1 (HIV-1) can be activated in a chronically infected T-cell line (ACH2 cells) by a cytokine, human tumor necrosis factor alpha (TNF-alpha). TNF-alpha treatment of ACH2 cells resulted in an increase in steady-state levels of HIV RNA and HIV transcription. Gel mobility shift assays demonstrated that the transcriptional activation of the HIV long terminal repeat (LTR) by TNF-alpha was associated with the induction of a nuclear factor(s) binding to the NF-kappa B sites in the LTR. Deletion of the NF-kappa B sites from the LTR eliminated activation by TNF-alpha in T cells transfected with plasmids in which the HIV LTR directed the expression of the bacterial chloramphenicol acetyltransferase gene. Thus, TNF-alpha appears to activate HIV RNA and virus production by ACH2 cells through the induction of transcription-activating factors that bind to the NF-kappa B sequences in the HIV LTR.

MeSH terms

  • Base Sequence
  • Cell Line
  • DNA, Viral / genetics*
  • DNA, Viral / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Genes, Viral* / drug effects
  • HIV-1 / drug effects
  • HIV-1 / genetics
  • HIV-1 / growth & development*
  • Humans
  • Molecular Sequence Data
  • Nuclear Proteins / metabolism
  • Protein Binding
  • Regulatory Sequences, Nucleic Acid
  • Repetitive Sequences, Nucleic Acid
  • Transfection
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Virus Activation*


  • DNA, Viral
  • DNA-Binding Proteins
  • Nuclear Proteins
  • Tumor Necrosis Factor-alpha