Transactivation of the HIV-1 LTR by HSV-1 immediate-early genes

Virology. 1992 Feb;186(2):788-91. doi: 10.1016/0042-6822(92)90048-t.

Abstract

Herpes simplex virus type 1 (HSV-1) activates transcription from the long terminal repeat (LTR) promoter region of the human immunodeficiency virus type 1 (HIV-1). HSV-1 immediate-early (IE) genes ICP0 and ICP4 are thought to be important mediators of this process, which is known to involve the induction of the cellular activators NF-kappa B and Sp1. We demonstrate that ICP0 and ICP4 transactivation of the LTR is largely dependent on the presence of NF-kappa B and Sp1 binding sites. However, in Jurkat CD4-positive lymphocytes, HSV-1 activates LTR constructs lacking all NF-kappa B or Sp1 Binding sequences. This effect is still evident when all sequences upstream of the TATA motif are removed. Such enhancer-independent transactivation can be produced by cotransfection of ICP0 and ICP4. Thus HSV-1 IE genes transactivate the HIV-1 LTR both through the induction of NF-kappa B and Sp1 and through another as yet undefined cellular factor.

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • Cloning, Molecular
  • DNA, Viral
  • Gene Expression Regulation, Viral
  • HIV Long Terminal Repeat / genetics*
  • Humans
  • Immediate-Early Proteins*
  • Molecular Sequence Data
  • Simplexvirus / genetics*
  • Simplexvirus / physiology
  • Transcriptional Activation*
  • Ubiquitin-Protein Ligases
  • Viral Proteins / genetics*
  • Viral Regulatory and Accessory Proteins / genetics
  • Virus Replication / genetics

Substances

  • DNA, Viral
  • IE1 protein, Human herpesvirus 1
  • Immediate-Early Proteins
  • Viral Proteins
  • Viral Regulatory and Accessory Proteins
  • herpes simplex virus, type 1 protein ICP4
  • Ubiquitin-Protein Ligases
  • Vmw110 protein, Human herpesvirus 1