The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response

FEBS Lett. 2011 Nov 16;585(22):3549-54. doi: 10.1016/j.febslet.2011.10.018. Epub 2011 Oct 19.

Abstract

Latent HIV-1 (human immunodeficiency virus-1) provirus is unaffected by current AIDS (acquired immunodeficiency syndrome) therapies. We show here that chaetocin, an SUV39H1 histone methyltransferase inhibitor, causes 25-fold induction of latent HIV-1 expression, while producing minimal toxicity and without causing T cell activation. Induction is associated with loss of histone H3 lysine 9 (H3K9) trimethylation at the long terminal repeat (LTR) promoter, and a corresponding increase in H3K9 acetylation. The effect of chaetocin is amplified synergistically in combination with histone deacetylase (HDAC) inhibitors. These results indicate that chaetocin may provide a therapy to purge cells of latent HIV-1, possibly in combination with other chromatin remodeling drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Chromatin Assembly and Disassembly
  • Drug Synergism
  • HIV Long Terminal Repeat
  • HIV-1 / drug effects*
  • HIV-1 / genetics
  • HIV-1 / metabolism
  • Histone Deacetylase Inhibitors / pharmacology*
  • Histones / metabolism
  • Humans
  • Jurkat Cells
  • Methylation
  • Methyltransferases / antagonists & inhibitors*
  • Methyltransferases / metabolism
  • Piperazines / pharmacology
  • Repressor Proteins / antagonists & inhibitors*
  • Repressor Proteins / metabolism
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Virus Activation
  • Virus Latency / drug effects

Substances

  • Histone Deacetylase Inhibitors
  • Histones
  • Piperazines
  • Repressor Proteins
  • chaetocin
  • SUV39H1 protein, human
  • Methyltransferases