Figure 3.

The role of EBI2 in antigen-driven B cell differentiation and in the lifecycle of EBV. Upon a successful lytic infection, EBV establishes a persistent infection in memory B cells. This has been proposed to be achieved by either direct infection of these cells (not shown in this figure) or by mimicking the antigen-driven B-cell differentiation into memory cells ⁵². (A) Antigen-activated naive B cells differentiate into highly proliferating B-cell blasts by the help of T cells. B-cell blasts then enter the follicles, where they expand to form GCs. Within the GCs, activated B cells undergo affinity maturation and proliferation upon antigen recognition on the surface of dendritic cells and stimulation by T cells. Finally, resting memory B cells enter the peripheral circulation. (B) During lytic EBV infection, virus-infected B cells proliferate and ensure virus spreading. Upregulation of EBI2 may ensure avoidance of the hostile environment of the GCs. (C) During latent EBV infection, EBV has been proposed to induce and regulate expression of viral proteins and host proteins to mimic the immune signals that promote B-cell differentiation ⁵². The EBI2 expression level is indicated by ++,+,-, and ? (if unknown).