Fig. 3

EBV infection and inflammation. EBV engages in an interaction with B lymphocyte through its gp220/350 receptors to B cell surface glycoprotein CD21. This interaction facilitates acute infection of EBV in B cells (#1), which subsequently causes transformation to B cell lymphoblastoid cells. After that, these lymphoblastoid B cells undergo cytolysis (#2) by NK cells, CD8⁺, and CD4⁺ T cells. Some B cells escape that cytolytic process and go to the latency (#3). During the late stage of life, virus reactivation (# 4) might occur followed by virus shedding, and secondary infection to Th1 cells. These reactivated and infected B and T cells possibly enter to CNS through BBB, and potentially engage in a microglial activation to induce inflammatory reactions (#5)