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

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • Wendy Bernhard
  • Kris Barreto
  • Amy Saunders
  • Matthew S Dahabieh
  • Pauline Johnson
  • Ivan Sadowski
<mark>Journal publication date</mark>16/11/2011
<mark>Journal</mark>FEBS Letters
Issue number22
Number of pages6
Pages (from-to)3549-54
Publication StatusPublished
<mark>Original language</mark>English


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.