Epigenetic control of the Epstein-Barr lifecycle.

Epstein-Barr virus (EBV) infects 95% of adults worldwide, causes infectious mononucleosis, is etiologically linked to multiple sclerosis and is associated with 200 000 cases of cancer each year. EBV manipulates host epigenetic pathways to switch between a series of latency programs and to reactivate from latency in order to colonize the memory B-cell compartment for lifelong infection and to ultimately spread to new hosts. Here, we review recent advances in the understanding of epigenetic mechanisms that control EBV latency and lytic gene expression in EBV-transformed B and epithelial cells. We highlight newly appreciated roles of DNA methylation epigenetic machinery, host histone chaperones, the Hippo pathway, m6A RNA modification and nonsense mediated decay in control of the EBV lifecycle.