The Long and Complicated Relationship between Epstein-Barr Virus and Epithelial Cells

Abstract

The roles of epithelial cells in infection and persistence of the Epstein-Barr virus (EBV) have long been difficult to resolve. However, recent developments have reinforced the conclusion that these cells are a major site of virus replication and raised the possibility that, like papillomaviruses, EBV has evolved to take advantage of epithelial differentiation to ensure survival, persistence, and spread.

Keywords: Epstein-Barr virus; epithelial cells; tropism.

FIG 1

Possible routes for infection and spread of EBV in vivo. 1. Cell-free virus particles produced by a transferred B cell, or that use an uninfected B cell as a transfer vehicle, infect the apical surface of the epithelium and spread through the epithelium to emerge as highly lymphotropic virus particles. 2. Virus particles infect B cells and establish latency in the memory B cell compartment. 3. Terminal differentiation of a B cell into a plasmablast induces reactivation and production of virus particles, which are epitheliotropic and infect basal epithelial cells to establish latency. 4. As basal cells differentiate, they can support productive replication and shed virus particles into saliva for transmission to a new host or for replenishing the reservoir in the existing host.