Epstein Barr virus infection induces tissue-resident memory T cells in mucosal lymphoid tissues

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Abstract Epstein Barr virus (EBV) contributes to around 2% of all tumors worldwide. Simultaneously, more than 90% of healthy human adults persistently carry EBV without clinical symptoms. In most EBV carriers it is thought that virus-induced tumorigenesis is prevented by cell-mediated immunity. Specifically, memory CD8 + T cells recognize EBV-infected cells during latent and lytic infection. Using a symptomatic primary infection model, similar to infectious mononucleosis (IM), we found EBV induced CD8 + tissue resident memory T cells (TRMs) in mice with a humanized immune system. These human TRMs were preferentially established after intranasal EBV infection in nasal-associated lymphoid tissues (NALT), equivalent to tonsils, the primary site of EBV infection in humans. They expressed canonical TRM markers, including CD69, CD103 and BLIMP-1, as well as Granzyme B, CD107a and CCL5, while demonstrating reduced CD27 expression and proliferation by Ki-67 expression. Despite cytotoxic activity and cytokine production ex vivo , these TRMs failed to control EBV viral loads in the NALT during infection although effector memory T cells (TEMs) controlled viral titers in spleen and blood. Overall, TRMs in mucosal lymphoid tissues are established by EBV infection, but primarily systemic CD8 + T cell expansion seems to attenuate viral loads in the context of IM-like infection.

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