Hodgkin's disease and the Epstein-Barr virus

Abstract

Hodgkin's disease is an unusual cancer because the malignant cells constitute only a minority of the total tumour mass and, as a consequence, the study of these cells has been a major challenge. Recently, the application of newer technologies, such as single cell polymerase chain reaction (PCR) and gene expression array analysis, to the study of Hodgkin's disease have yielded new insights into the pathogenesis of this tumour. In addition, the recognition that a proportion of Hodgkin's disease tumours harbour the Epstein-Barr virus (EBV) and that its genome is monoclonal in these tumours suggests that the virus contributes to the development of Hodgkin's disease in some cases. This review summarises current knowledge of the pathogenesis of Hodgkin's disease with particular emphasis on the association with EBV.

Epstein-Barr virus–associated lymphoproliferative disorders

“…Sex and ethnicity are also factors in the epidemiology of EBV-positive Hodgkin cases, where males from a Hispanic or Asian (Chinese) origin tend to be more commonly affected [12,30]. A bimodal age distribution has been recognized for EBV-positive Hodgkin lymphoma patients; children and the older-age group tend to have much higher rates than young adults, the explanation of which may rely on the more competent immune surveillance in young adults as compared with the less developed or declined immune system in children and older individuals, respectively [30].…”

Lymphoid Hyperplasia Resulting in Immune Dysregulation Is Caused by Porcine Reproductive and Respiratory Syndrome Virus Infection in Neonatal Pigs

“…However, cell number and IgG levels are not criteria for polyclonality because single clones can give rise to increased numbers of B cells and raise Ig levels, as in the case of lymphomas (29). EBV infection is known to be associated with the development of Hodgkin's lymphoma, which involves the expansion of a monoclonal B cell population (30). Therefore, the possibility that increased B cell numbers observed during PRRSV infection (28) result from the expansion of a monoclonal B cell population cannot be excluded.…”

The Human Leukocyte Antigen Class I Region Is Associated with EBV-Positive Hodgkin's Lymphoma: HLA-A and HLA Complex Group 9 Are Putative Candidate Genes

“…The majority of the tumor mass consists of an inflammatory infiltrate containing varying amounts of T (CD4 + and CD8 + ) and B lymphocytes, plasma cells, histiocytes, and eosinophilic granulocytes (1)(2)(3)(4). The Hodgkin/Reed-Sternberg cells and their neighboring cells are able to cross-talk via a complex of cytokine and cell contactdependent interactions, and these probably include proliferative and antiapoptotic signals favoring tumor cell survival and expansion (4,5). This suggests that immunologic mechanisms contribute to Hodgkin's lymphoma pathogenesis.…”