Abstract
Epstein-Barr virus (EBV) is a ubiquitous human herpes virus which is found as a predominantly asymptomatic infection in all human communities. Primary EBV infection usually occurs in childhood and, once infected, individuals become life-long virus carriers. The virus is the causative agent of infectious mononucleosis (IM), a self-limiting lymphoproliferative disease resulting from delayed primary EBV infection, and is also associated with a number of malignant tumours, including Burkitt’s lymphoma (BL) and lymphomas arising in immunocompromised patients (Miller, 1990). The B lymphotropic nature of EBV is evidenced by its association with these lymphoproliferations and by the ability of the virus to immortalise normal resting B lymphocytes in vitro, converting them into permanently growing lymphoblastoid cell lines (LCLs) (Nilsson et al., 1971). When peripheral blood lymphocytes from EBV seropositive individuals are placed in culture, the few virus-infected B-cells that are present regularly give rise to spontaneous outgrowth of EBV-transformed LCLs provided that immune T-cells are either removed or inhibited by addition of cyclosporin A to the culture (Rickinson et al., 1984). This phenomenon highlights the importance of EBV-specific cytotoxic T lymphocytes (CTLs) in controlling EBV-induced B-cell transformation (Fig. 1).
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Young, L.S., Niedobitek, G. (1995). Epstein-Barr Virus and Lymphomas: An Overview. In: Jarrett, R.F. (eds) Etiology of Hodgkin’s Disease. NATO ASI Series, vol 280. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0339-8_4
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