Abstract
The Epstein-Barr virus (EBV) establishes persistent latent infection in peripheral blood memory B cells, may cause infectious mononucleosis, and is associated with cancers including endemic Burkitt's lymphoma (BL). Although latent EBV transforms B cells in vitro, additional factors including immunocompromised status or, as in endemic BL, a co-infection with the malaria parasite Plasmodium falciparum seem to be required for the development of EBV-associated cancers. Toll-like receptors (TLRs) like TLR9 are capable to recognize EBV and launch innate immune responses, which may limit the spread of the virus and may contribute to control outgrowth of latently EBV-infected B cells. On the other hand, EBV may interfere with the expression and functionality of TLR9, thereby manipulating host immune responses towards favoring long-term survival of the virus. Triggering of TLR9 by bacterial, viral or P. falciparum DNA may impact on the proliferation of EBV-infected B cells and on the balance between latent and lytic EBV. Thus, TLR9 signaling in EBV-infected B cells may be beneficial for the host but also for the highly adapted human gammaherpesvirus EBV.
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