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

Abstract

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 virus-associated 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 define 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.