High RNA polymerase II occupancy on herpes simplex virus 1 late genes early in infection suggests progression to elongation is a critical switch to trigger late viral gene expression

We report the PRO-seq data generated from our analysis of RNA Polymerase II location along the HSV-1 genome at 3 and 6 hpi. This data set includes analysis of the 3hr time point in cells infected in the presence of cycloheximide and the 6hr time point in cells infected in the presence of phosphonoacetic acid, flavopiridol and acyclovir. We have compared the data set to a cytoplasmic mRNA seq data set which is also included. This consisted of polyadenylated, cytoplasmic RNA analyzed at 3 and 6 hpi post infection. Here we are depositing the results from this analysis providing the raw data sequence files along with our bigwig files produced when aligning it to a concatenated genome file containing the drosophila dm3 genome build, the human hg38 genome build, and the included HSV-1 (F-strain) genome with the external repeat sequences deleted. This data provides a nucletide-resolution map of RNA Pol II location in all of the described conditions. By comparing differences between cytoplasmic mRNA production and between Pol II occupancy patterns between samples, we have been able to discern that HSV-1 transcription is a highly regulated process, that involves mechanisms downstream of RNA Pol II recruitment to a HSV-1 promoter region. Overall design: PRO-seq analysis in HSV-1 infected HeP2 cells at 3 hpi with and without cycloheximide, and at 3hpi with and without flavopiridol, phophonoacetic acid, and acyclovir. Cytoplasmic, mRNA transcript levels of HSV-1 gens was gathered by an mRNAseq analysis of HSV-1 polyadenylated, cytoplasmic transcript levels at 3 and 6 hpi. These levels were then correlated back to Pol II occupancy from the PRO-seq analysis.