Stress Flips a Chromatin Switch to Wake Up Latent Virus Daphne C. Avgousti, Matthew D. Weitzman  Cell Host & Microbe  Volume 18, Issue 6, Pages 639-641 (December 2015) DOI: 10.1016/j.chom.2015.11.011 Copyright © 2015 Elsevier Inc. Terms and Conditions

Figure 1 Schematic Illustrating the Correlation between Heightened Stress and Increased HSV Gene Expression and Reactivation Initially, the episomal viral genome is coated with repressive chromatin marks such as H3K9me3 at promoters. As stress increases, the JNK signaling pathway is activated and phosphorylation on H3S10 allows transcription of viral genes without the removal of H3K9me3, passing the threshold for reactivation. With an increase in transcription of viral genes such as VP16, the reactivation enters Phase II with the re-writing of active marks such as H3K9ac on the viral genomes, viral replication, and progeny production. Cell Host & Microbe 2015 18, 639-641DOI: (10.1016/j.chom.2015.11.011) Copyright © 2015 Elsevier Inc. Terms and Conditions