Inhibition of the enzymatic activity of HDAC-1 and
likely HDAC-2 and 3 by synthetic inhibitors of HDACs
(HDACi) leads to activation of the HIV-1 LTR and HIV-1 gene
expression. Moreover, unlike cell activators of NFkB, such as
IL-2, OKT3, or TNFa, HDACi facilitate gene expression
without general activation cytokines and the T cell
In vitro, various HDACi induce HIV-1 gene expression
from latently infected cells line.27–29 Valproic acid (VPA), a
carboxilate HDACi prescribed for seizures and psychiatric
disorders, has been combined with HAART in small clinical
trials but without the desirable significant decrease of the latent
reservoir.26,30–32 The studies with VPA, a nonspecific weak
HDACi, have not resolved the potential of HDACi to purge
the virus.