Contribution of the Microenvironment to the Pathogenesis of EBVPositive Hodgkin and Nasal NKTcell Lymphomas

Eva Klein, Miki Takahara*, and Lorand Levente Kis

Abstract Depending on the differentiation and maturation of the EBV-carrying cell the virally encoded proteins can be expressed in various assortments. The expression of these proteins determines the fate of the EBV-harboring cell. Expression of the six nuclear and three membrane-associated EBV-encoded proteins, designated Type III latency, induces cell proliferation. This occurs only in B lymphocytes. In spite of the transforming capacity of EBV, humans are virus carriers without the emergence of B-cell malignancy, because the immune system recognizes and eliminates the cells which express the growth-promoting proteins. However, immunosuppressed individuals have a high risk for EBV-induced B-cell malignancies.

In EBV-associated malignancies of other cell types, such as Hodgkin and NK/ T-cell lymphomas, the expression of virally proteins is restricted. EBV does not induce the autonomous proliferation of the cells. However, it induces phenotypical changes that influence the fate of the cell. The virally encoded genes function in evasion of apoptosis, induction of cellular interactions, production and response to cytokines. Contribution of the microenvironment to the survival and proliferation of the EBV-carrying malignant cells is thus pivotal in these tumors.

Keywords Epstein-Barr virus, Hodgkin lymphoma, NK/T-cell lymphoma, microenvironment, cytokine

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