Journal
CELL HOST & MICROBE
Volume 18, Issue 6, Pages 639-641Publisher
CELL PRESS
DOI: 10.1016/j.chom.2015.11.011
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Funding
- NCI NIH HHS [T32 CA115299] Funding Source: Medline
- NIGMS NIH HHS [F32 GM112414] Funding Source: Medline
- NINDS NIH HHS [R01 NS082240, NS082240] Funding Source: Medline
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Stress-induced reactivation of latent herpesviruses requires disabling of repression, but the mechanism for converting silenced chromatin into an active state is unknown. In this issue of Cell Host & Microbe, Cliffe et al. (2015) suggest a methyl/phospho switch on histone H3 overcomes repression to facilitate reactivation of latent herpes simplex virus type 1 (HSV-1).
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