Abstract

Epstein-Barr virus (EBV) ubiquitously infects human beings and is associated with several malignancies. However, the mechanism of the viral oncogenicity remains largely to be understood. In our investigations, we have reported a tumor model in which that EBV facilitated the tumorigenesis in epithelial cells latently infected by EBV genome. Using this model, we have found several clues and further confirmed them for the viral pathogenesis. We have recently reported that the EBV copy number is related with the potential malignancy of the infected cells, corresponding to the activation level of LMP1 and NF-κB signaling. Though the DNA load in patient blood has been well-documented as an potential indicator of EBV-related diseases, this was the first experimental model to verify that the EBV copy number in cancer cells directly correlates with the tumorigenesis. We emphasize that not only “with or without” but also “more or less” should be concerned in EBV-related approaches at gene expression level or in genome context.

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