The functional interaction between Epstein–Barr virus and MYC in the pathogenesis of Burkitt lymphoma

Abstract

The Epstein-Barr virus (EBV) infection does not induce any apparent pathology in most people but it has been associated with an increased risk of developing a number of non-malignant diseases (e.g., infectious mononucleosis and multiple sclerosis) and some cancers. Among these, the association between EBV and Burkitt lymphoma (BL) is striking, involving a tumor where MYC is deregulated by translocation in all cases. BL is more prevalent in children from equatorial Africa (>90% of the cases) whereas the association of EBV with BL is much lower (25-40%) in other regions. This high association suggests that EBV is a driving mechanism, but whether it is sufficient to trigger lymphomagenesis or it is a cooperative factor is under debate. Indeed, the precise molecular mechanisms underlying the virus activity in infected B cells in collaboration with MYC is still unclear. The molecular mechanisms by which EBV operates in tumor B cells will be discussed.