The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes (Omni-ATAC-seq III)

We report that HSV-1 gives rise to transposase accessible chromatin in gene downstream areas, in regions that show transcription termination defects. We show that the viral protein ICP22 is responsible for this open chromatin. We used BAC-derived strain 17 HSV-1 WT and US1 deletion mutant and examined the opening of chromatin downstream of transcription termination sites of affected genes. Two biological replicates of cells infected with MOI 10 of the indicated viruses.