BRD4 and disease arising from reactivation of latent virus: In both cases, it depends on BRD4: disrupting E2:BRD4 with a dominant-negative BRD4 C-terminal peptide blocks the transactivation function of many PV E2 proteins; conversely, BRD4 knockdown reduces E2’s ability to repress genes that regulate the transition between lytic and latent infection [67,90,91,92].