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Virologica Sinica, 32 (3) : 175, 2017
Review
An update: Epstein-Barr virus and immune evasion via microRNA regulation
1. The Key Laboratory of Carcinogenesis of the Chinese Ministry of Health, Xiangya Hospital, Central South University, Changsha 410080, China
2. Cancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha 410078, China
3. Department of Microbiology, School of Basic Medical Sciences, Central South University, Changsha 410078, China
 Correspondence: jianhlu@csu.edu.cn
(843.80KB)  
Abstract
Epstein-Barr virus (EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans.To ensure its survival and maintain its B cell transformation function,EBV has developed powerful strategies to evade host immune responses.Emerging evidence has shown that microRNAs (miRNAs) are powerful regulators of the maintenance of cellular homeostasis.In this review,we summarize current progress on how EBV utilizes miRNAs for immune evasion.EBV encodes miRNAs targeting both viral and host genes involved in the immune response.The miRNAs are found in two gene clusters,and recent studies have demonstrated that lack of these clusters increases the CD4+ and CD8+ T cell response of infected cells.These reports strongly indicate that EBV miRNAs are critical for immune evasion.In addition,EBV is able to dysregulate the expression of a variety of host miRNAs,which influence multiple immune-related molecules and signaling pathways.The transport via exosomes of EBV-regulated miRNAs and viral proteins contributes to the construction and modification of the inflammatory tumor microenvironment. During EBV immune evasion,viral proteins,immune cells,chemokines,pro-inflammatory cytokines,and pro-apoptosis molecules are involved.Our increasing knowledge of the role of miRNAs in immune evasion will improve the understanding of EBV persistence and help to develop new treatments for EBV-associated cancers and other diseases.
Received: 8 Apr 2017  Accepted: 8 Apr 2017  Published online: 26 Jun 2017
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