Once inside the host, the herpes simplex virus remains as a latent infection through out the life of the host.
The DNA genome of HSV is silent during latency. A connection has now been established between cellular stress and the reactive expression of the genes creating herpes symptoms through infective virus particles.
“Cliffe et al. report that signaling through the c-Jun N-terminal kinase (JNK) pathway, which is activated in response to various types of cellular stress, relieved transcriptional repression of latent HSV.”