[Regulation and evasion of host immune responses by Epstein-Barr virus]

Epstein-Barr virus (EBV) is the first identified human oncogenic DNA virus in the gamma-herpesvirus family. EBV triggers a cascade events of innate immune responses through Toll-like receptor signaling including the production of type I interferons and the activation of functional autophagy. However, EBV has developed much more elaborate and sophisticated strategies for subverting and escaping the host immune system, such as limiting its own gene expression, activing the host ubiquitin-specific protease system, and interfering ubiquitin modification. EBV impairs the host immune system, leading to lifelong persistent infections, which in turn result in the occurrence of EBV-associated diseases, such as nasopharyngeal carcinoma and infectious mononucleosis. Thus, to better understand the mechanisms regarding the infection latentency and oncogenicity of EBV invasion will be crucial for identifying potential immunotherapeutic targets for EBV- related diseases, such as infectious mononucleosis and nasopharyngeal carcinoma. In this article, we discuss the research advances regarding the virology and immunology of EBV in the modulation of the host immune response and evasion.