Adam W. Whisnant

This study shows HSV-1 infection causes a downstream shift of +1 nucleosomes by depleting RNA Polymerase II from host genes, similar to Pol II depletion in yeast.

Heterogeneity-seq identifies causal factors driving heterogeneous cellular responses by combining single-cell RNA-seq with metabolic labeling and double machine learning.

This study shows HSV-1 inhibits phosphorylation of RNA polymerase II CTD serine-7, affecting viral gene expression and host transcription.

This study shows HSV-1 infection causes a downstream shift in promoter-proximal Pol II pausing for most host genes, more pronounced than NELF depletion.

The paper shows HSV-1 and influenza infection induce circular and linear splicing of the NEAT1_2 isoform, independent of vhs and linked to transcription termination disruption.

This study shows HSV-1 infection causes widespread changes in host mRNA alternative polyadenylation, with ICP27 playing a role in shifting polyadenylation to intronic sites and affecting mRNA export and expression.