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Annals of Oncology 7:S11-S17, 1996
© 1996 European Society for Medical Oncology

Reviews

The role of Epstein—Barr virus in the pathogenesis of Hodgkin's disease

G. Niedobitek

Institute for Cancer Studies and Department of Pathology, University of Birmingham Birmingham, UK.

Correspondence to: Dr. Gerald Niedobitek Institute for Cancer Studies Department of Pathology University of Birmingham, Birmingham B15 2TT, U.K.

Hodgkin's disease represents a phenotypically and genotypically heterogeneous lymphoma of CD30-positive tumour cells. Infection of the putative tumour cell population with Epstein-Barr virus (EBV) represents the most common genetic abnormality detectable in HD, yet the role of EBV in the pathogenesis of HD is only poorly understood. In virusassociated HD cases, monoclonal EBV genomes are detectable in all Hodgkin and Reed-Sternberg (HRS) cells, indicating that EBV infection takes place before expansion of the HRS cell population and, by implication, supporting the concept of a monoclonal origin of HRS cells. EBV infection does not dethie a distinct subgroup of HD but is detectable in different histotypes and in HRS cells expressing lymphocyte differentiation antigens of different cell lineages. Through the EBV-encoded protein, LMP1, the virus may superimpose an activated phenotype on genotypically immature lymphocytes. EBV-induced modulation of the cytokine expression pattern of HRS cells may contribute to the local inhibition of EBV-specific immunity observed in EBV-positive cases.

clonality, EBV, EBV-specific immunity, Hodgkin's disease, LMP1, tumour cell phenotype


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