Additionally, upon adenovirus infection, E1A sequestered pRb from E2F transcription factor and enhanced p300-mediated K873/K874 acetylation of pRb, acetylated form of which formed a ternary repressing complex with p300 and E1A to condense chromatin, resulting in specific repression of host genes with high p300 association that interfered with efficient virus infection, such as the TGFβ-, TNF-, and interleukin-signaling pathway components [145]. This evidence concerns the gene EP300 and viral infectious disease.