Recent studies using ATAC-seq and ChIP-seq have demonstrated that SARS-CoV-2 infection leads to decreased chromatin accessibility at IFN-β, ISG15, and IRF7 loci, correlating with increased levels of repressive histone marks such as H3K27me3 and reduced activating marks (H3K4me3, H3K27ac) at antiviral IFN gene loci, which correlates with silencing of antiviral genes transcription and blunted type I and III IFN responses early in infection (85). Here, IFNA1 is linked to infection.