Figure 3.

A hypothetical model of EBV role in breast carcinogenesis. Primary breast epithelial cells are susceptible to EBV infection, probably using EphA2 receptor. Once EBV latency is established, including EBNA-1, EBER and BART expression, the lytic switch can be activated. Xenobiotics may be involved in Zp activation as suggested in some models. BARF0 is involved in Her2/Her3 activation promoting tumor transformation by Ras/Raf/MEK/Erk and Pi3K/akt signaling pathways. BARF1 is involved in immune evasion and providing tumor properties. Xenobiotics or additional viral infections can cooperate with EBV for increasing breast tumor properties.