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. 2019 Nov 22;20(23):5861. doi: 10.3390/ijms20235861

Figure 2.

Figure 2

A model of EBV-infected plasma cell’s (PC) involvement in chronic oral infections. EBV-infected PCs (EBV+ PCs) infiltrate the site of the oral infection and actively produce EBV within a lesion. New viral particles infect neighboring epithelial cells (EC), which serve as an EBV pool. EBV+ PCs, aside of producing immunoglobulins, secret also pro-inflammatory cytokines and chemokines (IL1β, IL8, CXCL1, CXCL2), recruiting host immune players (natural killers (NK), helper T cells (CD4+), cytotoxic T cells (CD8+), etc.) to generate a pro-inflammatory reaction. Furthermore, the EBV infection can result in the emergence and proliferation of autoreactive B cells with “forbidden” epitopes favoring the production of autoantibodies and recruitment of T cells specific for lytic-cycle viral antigens with a further autoimmune attack. On the other side, EBV+ PCs may also produce anti-inflammatory cytokines (IL10, IL35) suppressing the host immune surveillance which leads to the superinfection of pathogenic bacteria. These bacteria, in turn, may reactivate the latent EBV and the production of new viral particles. And the circle starts anew leading to the progression of the infection [49,69,96,101,105].