Epigenetic Mechanisms in Latent Epstein-Barr Virus Infection and Associated Cancers.

Simple Summary: Epstein–Barr virus (EBV) was first isolated in 1964 and has since become an important human tumor virus. With an estimated 90% of the human population infected with the virus, EBV has also been shown to cause several types of cancers. The virus has evolved numerous epigenetic mechanisms by which it can affect its host and contribute to the development and progression of cancer. In this review, we introduce four prominent epigenetic regulatory mechanisms that result in host-virus interactions for the purpose of EBV infection, persistence, and contribution to EBV-associated diseases. We then look at how epigenetic profiles of the host are altered in EBV-associated cancers to understand the precise ways EBV interacts with its host to cause disease. This work explores the viral epigenetics of EBV and provides insights into the knowns and unknowns of research into EBV and EBV-associated cancers. The Epstein–Barr Virus (EBV) is a double-stranded DNA-based human tumor virus that was first isolated in 1964 from lymphoma biopsies. Since its initial discovery, EBV has been identified as a major contributor to numerous cancers and chronic autoimmune disorders. The virus is particularly efficient at infecting B-cells but can also infect epithelial cells, utilizing an array of epigenetic strategies to establish long-term latent infection. The association with histone modifications, alteration of DNA methylation patterns in host and viral genomes, and microRNA targeting of host cell factors are core epigenetic strategies that drive interactions between host and virus, which are necessary for viral persistence and progression of EBV-associated diseases. Therefore, understanding epigenetic regulation and its role in post-entry viral dynamics is an elusive area of EBV research. Here, we present current outlooks of EBV epigenetic regulation as it pertains to viral interactions with its host during latent infection and its propensity to induce tumorigenesis. We review the important epigenetic regulators of EBV latency and explore how the strategies involved during latent infection drive differential epigenetic profiles and host-virus interactions in EBV-associated cancers. [ABSTRACT FROM AUTHOR]