A model for Epstein–Barr virus (EBV) infection and persistence

A model for Epstein–Barr virus (EBV) infection and persistence
Eleni-Kyriaki Vetsika and Margaret Callan

Figure 1. A model for Epstein–Barr virus (EBV) infection and persistence. (a) In the oropharynx, EBV infects naive B cells and expresses the full spectrum of latent proteins (latency III programme: EBNA1, LMPs 1 and 2A, EBNA3s and LP). The virus can thereby drive the activation and proliferation of these B cells, which then migrate to lymphoid follicles and form germinal centres. Concomitantly, expression of EBNA3s and LP are downregulated, leaving EBNA1 and the LMPs expressed (latency II programme). Expression of the LMPs provides signals that allow the B cells to survive the germinal centre reaction and form resting memory B cells. (b) These resting memory B cells exit to the periphery. At this point, expression of other EBV proteins is downregulated, thereby allowing the virus to persist within the B cells but to evade a host immune response. Intermittent expression of EBNA1 within dividing B cells allows the virus genome to be distributed to each of the daughter B cells (latency I programme). (c) As B cells recirculate to the oropharynx, a switch into the EBV lytic cycle might occur, possibly triggered by maturation of B cells into plasma cells, allowing for virus replication, shedding into saliva and transmission both to new hosts and to previously uninfected B cells within the same host. This model is derived from work published by Thorley-Lawson and colleagues (Refs 11, 20, 21, 22, 23, 24, 31, 39).

Expert Reviews in Molecular Medicine: Vol. 6; Issue 23; 5 November 2004