Open AccessThe Histone Deacetylase Inhibitor ITF2357 Decreases Surface CXCR4 and CCR5 Expression on CD4+ T-Cells and Monocytes and is Superior to Valproic Acid for Latent HIV-1 Expression in Vitro
Author(s) -
Shay Matalon,
Brent E. Palmer,
Marcel F. Nold,
Anna Furlan,
Afework Kassu,
Gianluca Fossati,
Paolo Mascagni,
Charles A. Dinarello
Publication year - 2010
Publication title -
journal of acquired immune deficiency syndromes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.162
H-Index - 157
eISSN - 1944-7884
pISSN - 1525-4135
DOI - 10.1097/qai.0b013e3181d3dca3
Subject(s) - histone deacetylase inhibitor , valproic acid , in vitro , human immunodeficiency virus (hiv) , histone deacetylase , cxcr4 , histone deacetylase 2 , chemistry , pharmacology , biology , medicine , virology , histone , biochemistry , chemokine , epilepsy , receptor , psychiatry , gene
Chromatin-associated repression is one mechanism that maintains HIV-1 latency. Inhibition of histone deacetylases (HDAC) reverses this repression resulting in viral expression from quiescently infected cells. Clinical studies with the HDAC inhibitor valproic acid (VPA) failed to substantially decrease the latent pool within resting CD4(+) cells. Here we compared the efficacy of ITF2357, an orally active and safe HDAC inhibitor, with VPA for HIV-1 expression from latently infected cells in vitro. We also evaluated the effect of ITF2357 on the surface expression of CXCR4 and CCR5.