Integrins as triggers of Epstein-Barr virus fusion and epithelial cell infection

Abstract

Epstein-Barr virus is a ubiquitousorally-transmitted human herpesvirus that is carried by most of the adult population. It establishes latent infections in B lymphocytes, reactivates periodically from latency and can be amplified in epithelial cells where it is thought more commonly to undergo lytic replication. Entry into either cell involves fusion of the virus envelope with a cellmembrane. Fusion with a B cell requires four envelope glycoproteins, gB and aternary complex of gHgLgp42. Fusion is triggered by an interaction betweengp42 and HLA class II. Fusion with anepithelial cell requires three envelope glycoproteins, gB and a binary complex of gHgL. The presence of gp42 blocksinfection and blocks the interaction of gHgL with a specific receptor on the epithelial cell surface. We recently demonstratedthat both integrins v 6 and?v?8 can serve as specific receptors for gHgL and that on binding to gHgL, even in a soluble form, can provide the trigger for direct virus fusion with the epithelial cell plasma membrane. It reveals yet another way in which an integr in can beused by a pathogen to invade a cell. © 2010 Landes Bioscience.