Abstract
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).