NF-κB is activated after MTb engagement of PRRs [20], [66]. Multiple studies of HIV-1 activation have shown that initial recruitment of the NF-κB p50/p65 heterodimer to the HIV-1 proviral enhancer region is crucial for HIV gene transcription (reviewed in [67], [68]). Upon interaction with the viral LTR, NF-κB rapidly induces hyperacetylation of histones associated with nucleosome 1 (nuc-1) at the HIV-1 transcription start site, resulting in recruitment of the pTEFb complex, which is required for RNA pol II processivity ([69], reviewed in [68], [70]).