Activation of the human immunodeficiency virus long terminal repeat by herpes simplex virus type 1 is associated with induction of a nuclear factor that binds to the NF-κB/core enhancer sequence

J. M. Gimble, E. Duh, J. M. Ostrove, H. E. Gendelman, E. E. Max, A. B. Rabson

Research output: Contribution to journalArticlepeer-review

69 Scopus citations

Abstract

It has been previously shown that herpes simplex virus type 1 (HSV-1) infection of HeLa cells results in augmentation of gene expression directed by the human immunodeficiency virus (HIV) long terminal repeat (LTR). This effect is presumably mediated by protein interactions with the LTR. We have used two different assays of DNA-protein interactions to study the HSV-induced activation of the HIV LTR. Activation of the HIV LTR is associated with increased protein binding to LTR sequences in a region including the NF-κB/core enhancer and the Sp1 binding sequences as monitored by an exonuclease protection assay. Gel retardation assays demonstrated that HSV-1 infection resulted in the induction of a nuclear factor(s) that binds to the NF-κB/core enhancer sequence. In addition to the activation of the HIV LTR, HSV induction of NF-κB activity may be important for the regulation of HSV gene expression during a herpesvirus infection.

Original languageEnglish (US)
Pages (from-to)4104-4112
Number of pages9
JournalJournal of virology
Volume62
Issue number11
DOIs
StatePublished - 1988

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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