Epstein-Barr virus and Hodgkin's disease

Abstract

Epstein-Barr virus (EBV) has been identified by in situ hybridization studies in the Reed-Sternberg cells of Hodgkin's disease (HD) in approximately 40-50% of cases in most Western countries. Southern blot analysis has demonstrated a monoclonal pattern of infection, implying that the virus is present prior to clonal expansion. Immunohistochemical studies have consistently identified latent membrane protein-1 (LMP1) in the EBV- positive cases, and in combination with other studies, have demonstrated a type II latency pattern of infection. Polymerase chain reaction studies demonstrate a higher percentage of EBV-associated cases, but do not distinguish truly EBV-associated cases from cases in which in situ hybridization studies merely identify EBV within non-neoplastic lymphocytes. Deletions in the LMP1 gene have been identified in a subset of cases, although their significance is not yet known. EBV is most commonly associated with the mixed cellularity subtype of HD, is rarely found in nodular lymphocyte predominance, and is frequently associated with a neck presentation in stage 1 cases. To date, there is no correlation between EBV and cell lineage of the Reed-Sternberg cells, cytokine profile, patient stage, or clinical outcome. Although there is no correlation with p53 or bcl- 2 protein expression, there may be an inverse correlation between EBV- positivity and the identification of p53 mutations. EBV-associated cases are particularly common in HD occurring in developing countries, especially in the pediatric population. Almost all cases of HD occurring in the setting of human immunodeficiency virus infection are EBV-associated. In rare cases of HD complicating chronic lymphocytic leukemia, almost all cases have EBV within the Reed-Sternberg cells, suggesting a key role in the pathogenesis of these rare cases.

Publication Title

Gann Monographs on Cancer Research

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