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HIV-1 promoter activation following an oxidative stress mediated by singlet oxygen

S Legrand-Poels1, M Hoebeke, D Vaira

  • 1Laboratory of Virology, Institute of Pathology, University of Liège, Belgium.

Insights

Singlet oxygen (1O2) can activate the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) and reactivate latent HIV-1 infections. This oxidative stress can trigger viral replication, potentially impacting AIDS progression.

Area of Science:

  • Cellular biology
  • Molecular biology
  • Virology

Background:

  • Singlet oxygen (1O2) is a reactive oxygen species generated during various biological processes.
  • 1O2 can cause significant damage to cellular macromolecules, including DNA, and trigger cellular responses.
  • Oxidative stress is implicated in various diseases and cellular dysfunctions.

Purpose of the Study:

  • To investigate the genotoxic effects of singlet oxygen (1O2) on cellular systems.
  • To determine if 1O2 can activate the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR).
  • To examine the role of intracellularly and extracellularly generated 1O2 in HIV-1 reactivation.

Main Methods:

  • Exposure of epithelial cells with integrated HIV-1 LTR to 1O2.
  • Treatment of latently HIV-1 infected promonocytes and lymphocytes with intracellularly generated 1O2.
  • Assessment of HIV-1 LTR transactivation and viral reactivation.

Main Results:

  • Oxidative stress mediated by 1O2 transactivated the HIV-1 LTR in epithelial cells.
  • Intracellular 1O2 generation induced reactivation of latent HIV-1 in infected immune cells.
  • Extracellular 1O2 caused cell death but did not induce HIV-1 reactivation.

Conclusions:

  • Singlet oxygen acts as a genotoxic agent capable of activating HIV-1 gene expression.
  • Intracellular 1O2 can trigger the reactivation of latent HIV-1 infections.
  • These findings offer insights into the mechanisms of HIV-1 latency conversion and AIDS pathogenesis.

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