HE Epstein-Barr virus (EBV) was discovered 36 years ago by electron microscopy of cells cultured from Burkitt's lymphoma tissue by Epstein, Achong, and Barr. 1 Four years later, in 1968, EBV was shown to be the etiologic agent of heterophile-positive infectious mononucleosis. 2 EBV DNA was detected in tissues from patients with nasopharyngeal carcinoma in 1970. 3 In the 1980s, EBV was found to be associated with non-Hodgkin's lymphoma and oral hairy leukoplakia in patients with the acquired immunodeficiency syndrome (AIDS). 4,5 Since then, EBV DNA has been found in tissues from other cancers, including T-cell lymphomas and Hodgkin's disease. 6,7 EBV is one of the most successful viruses, infecting over 90 percent of humans and persisting for the lifetime of the person. EBV is closely related to viruses present in Old World nonhuman primates, including EBV-like viruses of chimpanzees and rhesus monkeys. For example, the rhesus monkey virus and EBV share similar sequences and genetic organization, and they maintain persistent infection in the oropharynx and in B cells. 8 Thus, EBV probably evolved from a nonhuman-primate virus.
VIROLOGIC FEATURES
Replication
EBV is a member of the herpesvirus family. The viral genome is encased within a nucleocapsid, which is, in turn, surrounded by the viral envelope. Before the virus enters the B cell, the major envelope glycoprotein, gp350, binds to the viral receptor, the CD21 molecule (the C3d complement receptor), 9 on the surface of the B cell. Other factors in addition to CD21 are important for infection. The ma-