- 作者: Ming-Chih Lai, Han-Hsiang Chen, Peng Xu and Robert Y. L. Wang
- 作者服務機構: 1. Department of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, 33302, Taiwan 2. Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, 33302, Taiwan 3. Department of Colorectal Surgery, Chang Gung Memorial Hospital at Linkou, Taoyuan, 33305, Taiwan 4. Xiangyang No.1 People’s Hospital, Hubei University of Medicine, Shiyan, Hubei Province, China 5. Division of Pediatric Infectious Disease, Department of Pediatrics, Chang Gung Memorial Hospital at Linkou, Taoyuan, 33305, Taiwan
- 中文摘要:
- 英文摘要:
Upon EV-A71 infection of a host cell, EV-A71 RNA is translated into a viral polyprotein. Although EV-A71 can use the cellular translation machinery to produce viral proteins, unlike cellular translation, which is cap-dependent, the viral RNA genome of EV-A71 does not contain a 5′ cap and the translation of EV-A71 protein is cap-independent, which is mediated by the internal ribosomal entry site (IRES) located in the 5′ UTR of EV-A71 mRNA. Like many other eukaryotic viruses, EV-A71 manipulates the host cell translation devices, using an elegant RNA-centric strategy in infected cells. During viral translation, viral RNA plays an important role in controlling the stage of protein synthesis. In addition, due to the cellular defense mechanism, viral replication is limited by down-regulating translation. EV-A71 also utilizes protein factors in the host to overcome antiviral responses or even use them to promote viral translation rather than host cell translation. In this review, we provide an introduction to the known strategies for EV-A71 to exploit cellular translation mechanisms. - 中文關鍵字:
- 英文關鍵字: Enterovirus A71, Translational control, Host factors, Gene expression