Chromatin organization of the HIV LTR in the setting of active HIV replication and HIV latency. In activated CD4+ T cells, histone acetyltransferases (HATs) hyperacetylate the nuc-1, resulting in remodeling of the chromatin structure. This allows for recruitment of Tat to the transactivation response element (TAR), relevant transcription factors and the RNA polymerase II (RNA Pol II), allowing for efficient viral transcription. In HIV latency, recruitment of HDACs leads to a reduction in acetylation of nuc-1 and inhibition of viral transcription.