Upon infection of susceptible cells, the RNA genome of the human immunodefi
ciency virus type 1 (HIV-1) is reverse transcribed into double-stranded DNA
, which can be subsequently integrated into the cellular genome. After inte
gration, the viral long terminal repeat (LTR) promoter is present in a nucl
eosome-bound conformation and is transcriptionally silent in the absence of
stimulation. Activation of HIV-1 gene expression is concomitant with an ac
etylation-dependent rearrangement of the nucleosome positioned at the viral
transcription start site. Thus, similar to most cellular genes, the transc
riptional state of the integrated HIV-1 provirus is closely linked to histo
ne acetylation. This enzymatic activity results from the function of histon
e-specific nuclear acetyltransferase (HAT) enzymes. Efficient viral transcr
iption is strongly dependent on the virally-encoded Tat protein. The mechan
ism by which Tat increases the rate of transcriptional initiation has been
recently demonstrated and involves the interaction of Tat with the transcri
ptional coactivator p300 and the closely related CREB-binding protein (CBP)
, having histone acetyltransferase activity.