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Abstract: Epstein-Barr virus (EBV) initiates infection by attaching to a specific cell receptor, CR2. This protein binds both the C3dg fragment of complement, which is presumably the physiologic ligand, and EBV (1). The importance of CR2 to normal B cell function is not clear, but several groups have implicated it in control of B cell activation. Antibodies to CR2, in concert with T cells (2) or T cell derived B cell growth factor (BCGF;3), induce proliferation and differentiation of the B cell. Cross linked human C3d, which binds to the equivalent receptor on the murine B cell, has been described as controlling the entry of B cells from G 1 into S phase (4). We, therefore, thought it of interest to determine whether, by virtue of its adaptation to bind to CR2, EBV has acquired the ability to mimic some of these effects. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.