HSV-1-induced disruption of transcription termination resembles a cellular stress response but selectively increases chromatin accessibility downstream of genes.

HSV-1-induced disruption of transcription termination resembles a cellular stress response but selectively increases chromatin accessibility downstream of genes.

Lytic herpes simplex virus 1 (HSV-1) infection triggers disruption of transcription termination (DoTT) of most cellular genes, resulting in extensive intergenic transcription. Similarly, cellular stress responses lead to gene-specific transcription downstream of genes (DoG). In this study, we perfor...

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Bibliographic Details
Main Authors: Thomas Hennig, Marco Michalski, Andrzej J Rutkowski, Lara Djakovic, Adam W Whisnant, Marie-Sophie Friedl, Bhaskar Anand Jha, Marisa A P Baptista, Anne L'Hernault, Florian Erhard, Lars Dölken, Caroline C Friedel
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-03-01
Series:PLoS Pathogens
Online Access:http://europepmc.org/articles/PMC5886697?pdf=render

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