Herpes Simplex Virus Reactivation Involves a Dual Leucine Zipper Kinase-Dependent Wave of Lytic Gene Expression That Is Independent of Histone Demethylase Activity and Viral Genome Synthesis.

Herpes simplex virus 1 (HSV-1) maintains a lifelong latent infection in neurons and periodically reactivates, resulting in the production of infectious virus. The exact cellular pathways that induce reactivation are not understood. In primary neuronal models of HSV latency, the cellular protein dual leucine zipper kinase (DLK) has been found to initiate a wave of viral gene expression known as phase I.

PML-NB-dependent type I interferon memory results in a restricted form of HSV latency.

Herpes simplex virus (HSV) establishes latent infection in long-lived neurons. During initial infection, neurons are exposed to multiple inflammatory cytokines but the effects of immune signaling on the nature of HSV latency are unknown. We show that initial infection of primary murine neurons in the presence of type I interferon (IFN) results in a form of latency that is restricted for reactivation.

Strength in diversity: Understanding the pathways to herpes simplex virus reactivation.

Herpes simplex virus (HSV) establishes a latent infection in peripheral neurons and can periodically reactivate to cause disease. Reactivation can be triggered by a variety of stimuli that activate different cellular processes to result in increased HSV lytic gene expression and production of infectious virus. The use of model systems has contributed significantly to our understanding of how reactivation of the virus is triggered by different physiological stimuli that are correlated with recrudescence of human disease.