One of the many conundrums of herpesvirology is why a herpesvirus is so proffigate in its use of four or more envelope glycoproteins for entry into a cell when other viruses can manage very well with only one or two. Proffigacy does, however, have its advantages. Epstein-Barr virus (EBV), originally recognized for its ability to infect and transform lymphocytes, is now clearly understood to infect epithelial cells as part of its normal cycle of persistence in a human host, and under some circumstances, the virus may infect T cells, natural killer cells, smooth muscle cells (47), and possibly monocytes as well (11, 50). Our understanding of how EBV enters each of these cell types is very incomplete, but some of the major players involved in B-cell and epithelial cell infections are being identified, and they provide a window into the ffexibility of tropism that the use of different combinations of virus and cell membrane proteins can provide. This review summarizes what we know about these players so far.