Infectious mononucleosis: model for self-limiting lymphoproliferation

Evidence for the extensive lymphoproliferation which characterises infectious mononucleosis (I.M.) is summarised, and some of the mechanisms which are though to control lymphoproliferative activity in this disease are discussed. The main host responses which appear to limit lymphoproliferation in I.M. include the development of humoral antibodies against the Epstein-Barr (E.B.) virus-associated membrane antigen (present on the E.B. viral envelope and on E.B.-virus-infected cells) and cellular immune responses directed against E.B.-virus-containing lymphocytes. Recent evidence is reviewed which indicates that E.B. virus preferentially infects B lymphocytes and that these E.B.-virus-containing cells, which are altered antigenically, evoke a massive response in the host T cells which do not carry E.B. virus; in the presence of E.B.-virus-infected B cells, T cells are transformed and become cytotoxic for B cells. Some of the general implications of the predominant T-cell response in I.M. are discussed with particular relation to autoantibody formation and antigenic competition. The possible role of the distinctive heterophil antigens and antibodies in determining the self-limiting course of I.M. is briefly considered. The general status of I.M. as a self-limiting, albeit intense, lymphoproliferative disease is appraised and the tenuous relationship between I.M. and irreversible lymphoproliferative states is discussed.