In the present study, we demonstrate an important role for histone H3 acetylation in the stimulation of IFN-A gene transcription during virus infection, and a functional involvement of HDAC3 in the post-induction repression of IFN-A gene transcription, acting via histone H3K9 and H3K14 deacetylation. The gene discussed is IFNA1; the disease is viral infectious disease.