DNA methylation and the Epstein-Barr virus

Abstract

EBV is a ubiquitous herpesvirus associated with a variety of lymphoid and epithelial tumors. In healthy lymphocytes and in tumors immune surveillance is evaded by suppression of a family of immunodeficient viral antigens. Methylation of a viral promoter plays a crucial role in this suppression. Methylation of the viral genome in the latent state over evolutionary time is believed to account for CpG suppression that distinguishes this virus from most other large DNA viruses. Pharmacologic manipulation of methylation may offer an opportunity to unmask viral antigens and expose tumors to immense surveillance.