HIV-1, HTLV-I and the interleukin-2 receptor: insights into transcriptional control

Haematol Blood Transfus. 1989;32:393-401. doi: 10.1007/978-3-642-74621-5_67.


In this study, we present direct evidence for the binding of the inducible cellular protein, HIVEN86A, to a 12-bp element present in the IL-2R alpha promoter. This element shares significant sequence similarity with the NF-kappa B binding sites present in the HIV-1 and kappa immunoglobulin enhancers. Transient transfection studies indicate that this kappa B element is both necessary and sufficient to confer tax or mitogen inducibility to a heterologous promoter. As summarized schematically in Fig. 5, the findings suggest that the HIVEN86A protein may play a central role in the activation of cellular genes required for T-cell growth, specifically the IL-2R alpha gene. In addition, the induced HIVEN86A protein also binds to a similar sequence present in the HIV-1 LTR leading to enhanced viral gene expression and ultimately T-cell death. Thus, mitogen activation of the HIV-1 LTR appears to involve the same inducible transcription factor(s) that normally regulates IL-2R alpha gene expression and T-cell growth. These findings further underscore the importance of the state of T-cell activation in the regulation of HIV-1 replication. Our results also demonstrate that HIVEN86A is induced by the tax protein of HTLV-I. Thus, in HTLV-I infected cells, normally the tight control of the transient expression of the IL-2R alpha gene is lost. The constitutive high-level display of IL-2 receptors may play a role in leukemic transformation mediated by HTLV-I (ATL). Apparently by the same mechanism, the tax protein also activates the HIV-1 LTR through the induction of HIVEN86A.(ABSTRACT TRUNCATED AT 250 WORDS)

MeSH terms

  • Base Sequence
  • Cell Line
  • Chromosome Mapping
  • DNA / metabolism
  • DNA-Binding Proteins / metabolism
  • HIV-1 / genetics*
  • Human T-lymphotropic virus 1 / genetics*
  • Humans
  • Molecular Sequence Data
  • Nuclear Proteins / biosynthesis
  • Promoter Regions, Genetic / physiology
  • Protein Binding
  • Receptors, Interleukin-2 / genetics*
  • Transcription Factors / metabolism
  • Transcription, Genetic*
  • Transfection / genetics


  • DNA-Binding Proteins
  • Nuclear Proteins
  • Receptors, Interleukin-2
  • Transcription Factors
  • DNA