Viral Regulation of RNA Granules in Infected Cells

作     者：Qiang Zhang Nishi R. Sharma Zhi-Ming Zheng Mingzhou Chen 

作者机构：State Key Laboratory of Virology and Modern Virology Research Center College of Life Sciences Wuhan UniversityWuhan 430072 China Tumor Virus RNA Biology Section RNA Biology Laboratory National Cancer Institute National Institutes of Health Frederick MD 21702 USA 

出 版 物：《Virologica Sinica》 (中国病毒学（英文版）)

年 卷 期：2019年第34卷第2期

页      面：175-191页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1002[医学-临床医学] 07[理学] 1001[医学-基础医学(可授医学、理学学位)] 

基　　金：supported by grants from the China Natural Science Foundation (81825015 and 31630086) the Natural Science Foundation of Hubei Province Innovation Group (2017CFA022) Intramural Research Program of NCI/NIH (1ZIASC010357 to ZMZ) 

主　　题：Stress granules (SG) P-bodies (PB) RNA virus - DNA virus 

摘      要：RNA granules are cytoplasmic, microscopically visible, non-membrane ribo-nucleoprotein structures and are important posttranscriptional regulators in gene expression by controlling RNA translation and stability. TIA/G3BP/PABP-specific stress granules(SG) and GW182/DCP-specific RNA processing bodies(PB) are two major distinguishable RNA granules in somatic cells and contain various ribosomal subunits, translation factors, scaffold proteins, RNA-binding proteins, RNA decay enzymes and helicases to exclude m RNAs from the cellular active translational pool. Although SG formation is inducible due to cellular stress, PB exist physiologically in every cell. Both RNA granules are important components of the host antiviral defense. Virus infection imposes stress on host cells and thus induces SG formation. However, both RNA and DNA viruses must confront the hostile environment of host innate immunity and apply various strategies to block the formation of SG and PB for their effective infection and multiplication. This review summarizes the current research development in the field and the mechanisms of how individual viruses suppress the formation of host SG and PB for virus production.