Epstein-Barr virus(EBV), a ubiquitous human double-stranded DNA virus, is associated with a variety of malignancies including Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma, and gastric carcinoma. Latent EBV infections have been discovered in cases of EBV -associated cancers, suggesting that EBV latent genes contribute to oncogenesis. Here, I describe mechanisms of oncogenesis associated with EBV, focusing on functions of EBV latent membrane protein(LMP)and EBV-encoded small RNA (EBER). LMP2A, which mimics B cell receptor signaling, and LMP1, which mimics CD40 signaling, collaboratively contribute to malignant lymphoma development. It has been reported that LMP2A-mediated intracellular signaling plays significant roles in epithelial carcinogenesis. However, it has also been demonstrated that EBER, which is expected to have a double-stranded RNA(dsRNA)structure, triggers signal transduction via host viral RNA sensors, RIG-I and TLR3, causing EBV-associated pathogenesis, including carcinogenesis.