Laboratory for Experimental Infectious Diseases and Cancer Research of the Division of Infectious Diseases and Hospital Epidemiology and the Division of Oncology, University of Zurich, 8032 Zurich, Switzerland.
Front Biosci (Landmark Ed). 2012 Jan 1;17(4):1219-31. doi: 10.2741/3982.
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.
EB 病毒（EBV）在周围血液记忆 B 细胞中建立持续潜伏感染，可能导致传染性单核细胞增多症，并与包括地方性伯基特淋巴瘤（BL）在内的癌症有关。尽管潜伏 EBV 在体外转化 B 细胞，但似乎需要其他因素，包括免疫功能低下状态，或如地方性 BL 中那样与疟原虫 Plasmodium falciparum 的共同感染，才能发展为 EBV 相关癌症。TLR9 等 Toll 样受体（TLRs）能够识别 EBV 并启动先天免疫反应，这可能限制病毒的传播，并有助于控制潜伏 EBV 感染的 B 细胞的过度生长。另一方面，EBV 可能会干扰 TLR9 的表达和功能，从而操纵宿主免疫反应，有利于病毒的长期存活。细菌、病毒或 P. falciparum DNA 触发 TLR9 可能会影响 EBV 感染的 B 细胞的增殖以及潜伏和裂解 EBV 之间的平衡。因此，EBV 感染的 B 细胞中的 TLR9 信号可能对宿主有益，但对高度适应的人类γ疱疹病毒 EBV 也有益。
