IFNA1 and infection: In contrast, infection of Calu3 with the highly pathogenic HPAI and MERS-CoV resulted in increased levels of H3K27me3 and decreased levels of H3K4me3 occupancy at the promoter regions of subsets of specific ISGs, which were not induced, demonstrating that these viruses have developed antagonistic mechanisms to specifically target the IFN arm of the innate immunity (Figure 4).