Cross-talk between Epstein-Barr virus and microenvironment in the pathogenesis of lymphomas.

Epstein-Bar virus (EBV) is known to directly drive the neoplastic transformation of lymphoid cells resulting in the development of a variety of lymphoproliferative disorders. Emerging evidence however indicates that this final outcome is also related to the ability of EBV to shape microenvironment making it more conducive to cell transformation. Indeed, EBV up-regulates the production of several soluble factors promoting the growth and/or the survival of lymphoid cells and orchestrates a variety of complex mechanisms favoring their escape from anti-tumor immune responses. Furthermore, EBV-infected B lymphocytes actively secrete exosomes and recent investigation is now shedding light on the content and functional impact that these bioactive vesicles may have in bystander recipient cells. The complex interplay existing between EBV-carrying lymphoid cells and tumor microenvironment is now offering attractive targets of therapy that can be exploited to improve current therapeutic strategies for EBV-driven lymphoid malignancies.
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