The Epstein-Barr virus (EBV) infects most humans.1 Nearly all infections of infants and children are asymptomatic, but about one third of infected adolescents and young adults develop acute infectious mononucleosis. A hallmark of that disease is the infiltration of blood and tissues with reactive T lymphocytes, denoting an exuberant, perhaps excessive, host response to the virus. In the setting of deficient immunity, acute EBV infections may present as aggressive, and even fatal, B-cell proliferative disorders.2
Whatever the clinical outcome of the initial exposure to EBV, it is certain that this herpesvirus persists for life in salivary glands and B lymphocytes. In a sense, these reservoirs of latent virus constitute a barometer of immune competence. The ability of EBV to reactivate, as reflected by rates of virus shedding in the saliva and levels of antibodies to EBV antigens, depends inversely on the integrity of the cellular immune system.