Abstract:
The observation by Epstein and Barr (EB) of virus particles in Burkitt lymphoma cells in 1964 led 4 years later to the discovery that this virus was the long sought agent responsible for infectious mononucleosis. Pathophysiologically the EB virus specifically infects B lymphocytes of the immune system and induces perpetual multiplication of these cells if infection remains uncontrolled. The T lymphocytes, once sensitized against these virus infected cells, either kill them or suppress their continuous growth. During acute infectious mononucleosis, these stimulated T cells appear in the bloodstream as atypical lymphocytes. If cell-mediated immunity is hampered by either congenital or acquired immunodeficiency the proliferative potential of EBV infected B lymphocytes may become uncontrolled and lead either to fulminant and lethal infectious mononucleosis or to polyclonal or monoclonal B cell proliferation. This later phenomenon appears to be the source of most of the lymphoma observed in transplant patients who are chronically immunosuppressed. Much remains to be understood of the mechanisms of EBV infections, which in some geographic areas lead to inapparent infections and in others to Burkitt lymphoma or nasopharyngeal carcinoma, while in temperate regions the clinical manifestations are those of infectious mononucleosis.
Keywords: Burkitt's Lymphoma/*ETIOLOGY English Abstract Female Herpesviridae Infections/*ETIOLOGY *Herpesvirus 4, Human Human Infectious Mononucleosis/*ETIOLOGY Male JOURNAL ARTICLE
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