Recent advances in understanding Epstein-Barr virus

Abstract

Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population. Infection with EBV is often asymptomatic but can manifest in a range of pathologies from infectious mononucleosis to severe cancers of epithelial and lymphocytic origin. Indeed, in the past decade, EBV has been linked to nearly 10% of all gastric cancers. Furthermore, recent advances in high-throughput next-generation sequencing and the development of humanized mice, which effectively model EBV pathogenesis, have led to a wealth of knowledge pertaining to strain variation and host-pathogen interaction. This review highlights some recent advances in our understanding of EBV biology, focusing on new findings on the early events of infection, the role EBV plays in gastric cancer, new strain variation, and humanized mouse models of EBV infection.

Keywords: EBV; Herpes simplex virus; Herpesvirus; gastric cancer.

Figure 1.. Initial events of Epstein-Barr virus (EBV) infection.

The EBV membrane glycoprotein gp42 binds to its cell surface receptor major histocompatibility complex class II (MHC-II) to initiate entry into the cell. Also, gp350/220 binds to its cell surface receptor CD21 for entry. Interaction with CD21 initiates signaling cascades that prime resting B cells for persistent latent infection. Following endocytosis, the virion and packaged tegument proteins are released into the cytoplasm following fusion of the virion membrane with endosomal membrane. In particular, BNRF1 disrupts the Daxx/ATRX repressor complex to facilitate viral gene expression.