Selective effects of DNA damaging agents on HIV long terminal repeat activation and virus replication in vitro. Academic Article uri icon

Overview

abstract

  • Much attention has recently focused on the observation that UV light can activate the long terminal repeat (LTR) of the human immunodeficiency virus (HIV). Although the mechanism of LTR activation remains obscure, several lines of investigation have suggested that it is a result of activation of the NF-kappa B transcription factor(s) following signaling events related to generalized DNA damage. In this report, we present data demonstrating that HIV LTR activation is not a general consequence of cellular DNA damage, but rather a process unique to specific genotoxic stimuli, and that it does not necessarily depend on activation of NF-kappa B. Furthermore, we demonstrate that several of these agents can significantly increase HIV replication and accelerate CD4-positive lymphocyte cytotoxicity in vitro. These findings, therefore, could have clinical significance to AIDS patients with malignancies who are undergoing radiotherapy and chemotherapy.

publication date

  • February 1, 1996

Research

keywords

  • Antineoplastic Agents
  • DNA Damage
  • DNA, Viral
  • HIV Long Terminal Repeat
  • HIV-1
  • Virus Activation
  • Virus Replication

Identity

Scopus Document Identifier

  • 1842510546

Digital Object Identifier (DOI)

  • 10.1097/00042560-199602010-00001

PubMed ID

  • 8556392

Additional Document Info

volume

  • 11

issue

  • 2