translation agency

NLM AIDSLINE
Transactivation of the HIV-1 LTR by HSV-1 immediate-early genes.
Margolis DM; Rabson AB; Straus SE; Ostrove JM; Medical Virology Section,
April 30, 1992
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

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