Epstein–Barr Virus-Associated Carcinogenesis

Dear colleague,

Epstein–Barr virus (EBV) is a persistent and widespread human gamma herpesvirus, infecting more than 90% of the adult human population. EBV is associated with several human malignancies including Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s disease, immunoblastic B lymphoma in AIDS patients, post-transplant-associated lymphomas, T-cell lymphomas, and some gastric carcinomas. Most modern theories of carcinogenesis consider the multi-step development of tumors, i.e., the theory that infection with a ubiquitous virus at the right time in the host life represents a step toward carcinogenesis, which seems to be tenable. However, the precise mechanisms of this EBV-mediated carcinogenesis are not yet clear.

After primary infection of B cells with EBV, infected B cells express several viral homologs of human genes that promote activation (LMP1 and CD40) or survival (BHRF and BCL2). In addition, EBV-infected B cells also induce various surface molecules such as CD70, CD77, B7 family molecules, germinal center markers, and adhesion molecules. In addition, EBV infection induces epithelial–mesenchymal transition in several epithelial cells. Recently EBV-encoded EBNA1 was shown to regulate cell viability by modulating miR34a–NOX2–ROS signaling in gastric cancer cells. The mechanisms underlying these various molecule-induced signaling events were found to differ from each other. These results provide a new concept for understanding various surface molecules expressed during EBV-induced transformation, and these newly defined molecules may be new potential targets for use in EBV-positive cancer therapy.

Prof. Dr. Jae Seung Kang
Prof. Dr. Dae Young Hur
Guest Editors

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• Epstein–Barr virus
• carcinogenesis
• epithelial–mesenchymal transition (EMT)
• apoptosis
• EBV-positive cancer