Epigenetic consequences of Epstein–Barr virus infection

Abstract

The biphasic nature of the Epstein–Barr virus (EBV) life cycle is tightly regulated by epigenetic modifications. Silencing of viral gene expression associated with latency is accompanied by repressive chromatin modifications and DNA methylation. Latency is integral to the lifelong persistence of EBV, yet persistence also relies on viral replication and virus production for infection of naïve hosts. Thus, EBV can overcome and disrupt the repressive epigenetic environment of the latent viral genomes. Viral modulators of the host epigenetic machinery are not only involved in establishing the latent and lytic viral epigenetic states but also reprogram the host epigenome in ways that are likely beneficial to the virus, but can carry long term consequences to the host. Here, we will review epigenetic aspects of EBV life cycle control and consequences to the host cell.