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


Virology. 1992 Feb;186(2):788-91. Unique Identifier : AIDSLINE

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.

Animal Base Sequence Cell Line Cloning, Molecular DNA, Viral Gene Expression Regulation, Viral Human HIV Long Terminal Repeat/*GENETICS Molecular Sequence Data Simplexvirus/*GENETICS/PHYSIOLOGY *Trans-Activation (Genetics) Viral Proteins/*GENETICS Viral Regulatory Proteins/GENETICS Virus Replication/GENETICS JOURNAL ARTICLE


Information in this article was accurate in April 30, 1992. The state of the art may have changed since the publication date. This material is designed to support, not replace, the relationship that exists between you and your doctor. Always discuss treatment options with a doctor who specializes in treating HIV.