Epstein-Barr virus (EBV) infection is associated with a range of autoimmune and lymphoproliferative syndromes (reviewed in Giller & Grosse 1989, Klein 1994, Khanna et al. 1995). EBV is known to trigger production of autoreactive antibodies against a variety of cellular tissues (reviewed in Vaughan 1995), but the mechanisms by which EBV infection results in autoimmune disorders are not well known. Postulated mechanisms include stimulation of antigen production by tissues damaged by EBV, or a direct response to viral proteins sharing some antigenic determinants with normal cellular proteins (Giller & Grosse 1989, Vaughan 1995). EBV genomic sequences have been demonstrated in T-cell tumors (Jones et al. 1988, Chen et al. 1993), suggesting that EBV infection of T lymphocytes occurs in vivo. More recent data also suggest a significant role for EBV-infected T lymphocytes in both acute infectious mononucleosis (AIM)(Anagnostopoulos et al. 1995) as well as in the hemophagocytic syndrome (Su et al. 1994). The EBV/C3d receptor is present on human thymocytes, peripheral T lymphocytes, and T-lym-