Skip to main content
. 2016 Aug 29;7:323. doi: 10.3389/fimmu.2016.00323

Figure 1.

Figure 1

Role of NK cells in the immune control of the EBV life cycle. Epstein–Barr virus (EBV) is transmitted via saliva exchange and infects submucosal B cells. In infected naïve B cells, the latency III EBV program can be found (EBNA1, 2, 3A–C, LP, and LMP1 and 2). Activation via EBV infection drives infected B cells into differentiation. In resulting germinal center B cells, latency II EBV infection can be found (EBNA1, LMP1 and 2). These EBV proteins allow EBV-infected B cells to survive and enter the memory B cell pool. In memory B cells, all EBV proteins expression is switched off (latency 0). Upon B cell receptor cross-linking, the lytic EBV cycle is activated due to plasma cell differentiation, which allows epithelial cell infection for further amplification of infectious virus before shedding into saliva. NK cells target lytically EBV replicating cells via their activating NKG2D and DNAM-1 receptors. It remains unclear if also lytically EBV replicating epithelial cells can be recognized by NK cells.