Epstein-Barr Virus Entry

The major players involved in moving EBV through a B-cell membrane have been identified, at least on the part of the virus. The model emerging is that gp350/220 binds to CR2, gp42 binds to HLA class II, and fusion is mediated by gHgL and gB. The possibility clearly exists, however, that there are additional cell partners for gHgL and gB. Some of the players involved in moving EBV through an epithelial cell membrane have been identified. Fusion involves gHgL and gB, but attachment may involve gp350/220, gHgL, or BMRF2, or possibly, if the virus is transferred from the surface of a B cell, no attachment receptor specific for any viral protein at all. With the possible exception of CR2, no cell partners have yet been identified on an epithelial cell, though there is clear evidence that they exist. There is also no conceptual understanding of the mechanism of fusion and very little insight into events inside the cell that may be triggered by interactions occurring at the cell surface. Much is still to be learned. Despite the incompleteness of our understanding, however, what we know already provides a fascinating glimpse into differential use of virus proteins and cell partners to manipulate virus tropism and influence virus trafficking between one cell compartment and another. EBV is associated with human malignancies, and primary infection in a minority of individuals causes acute, but self-limiting, mononucleosis. The majority of humans, however, live without incident with a virus that continually infects their lymphocytes and epithelial cells. The strategies that have evolved to make this possible also continue to be remarkable.