Oxaliplatin antagonizes HIV-1 latency by activating NF-κB without causing global T cell activation

Biochem Biophys Res Commun. 2014 Jul 18;450(1):202-7. doi: 10.1016/j.bbrc.2014.05.088. Epub 2014 May 27.

Abstract

Reactivation of latent HIV-1 is a promising strategy for the clearance of the viral reservoirs. Because of the limitations of current agents, identification of new latency activators is urgently required. Using an established model of HIV-1 latency, we examined the effect of Oxaliplatin on latent HIV-1 reactivation. We showed that Oxaliplatin, alone or in combination with valproic acid (VPA), was able to reactivate HIV-1 without inducing global T cell activation. We also provided evidence that Oxaliplatin reactivated HIV-1 expression by inducing nuclear factor kappa B (NF-κB) nuclear translocation. Our results indicated that Oxaliplatin could be a potential drug candidate for anti-latency therapies.

Keywords: HIV-1 latency; NF-κB transcription factor; Oxaliplatin; Synergistic reactivation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • HIV-1 / drug effects
  • HIV-1 / immunology*
  • Humans
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology*
  • NF-kappa B / immunology*
  • Organoplatinum Compounds / pharmacology*
  • Oxaliplatin
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / virology*
  • Virus Activation / drug effects
  • Virus Activation / immunology*
  • Virus Latency / drug effects
  • Virus Latency / immunology*

Substances

  • NF-kappa B
  • Organoplatinum Compounds
  • Oxaliplatin