调控肠道病毒感染过程中的蛋白稳态网络：EV-A71 和 EV-D68 的前馈机制。
Regulation of the proteostasis network during enterovirus infection: A feedforward mechanism for EV-A71 and EV-D68.
机构信息
Department of Biochemistry and Molecular Biology, College of Medicine, Chang Gung University, Kweishan, Taoyuan, Taiwan.
Department of Biochemistry and Molecular Biology, College of Medicine, Chang Gung University, Kweishan, Taoyuan, Taiwan; Research Center for Industry of Human Ecology and Graduate Institute of Health Industry Technology, Chang Gung University of Science and Technology, Taoyuan, Taiwan; Research Center for Emerging Viral Infections, College of Medicine, Chang Gung University, Kweishan, Taoyuan, Taiwan; Molecular Infectious Disease Research Center, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
出版信息
Antiviral Res. 2021 Apr;188:105019. doi: 10.1016/j.antiviral.2021.105019. Epub 2021 Jan 20.
The proteostasis network guarantees successful protein synthesis, folding, transportation, and degradation. Mounting evidence has revealed that this network maintains proteome integrity and is linked to cellular physiology, pathology, and virus infection. Human enterovirus A71 (EV-A71) and EV-D68 are suspected causative agents of acute flaccid myelitis, a severe poliomyelitis-like neurologic syndrome with no known cure. In this context, further clarification of the molecular mechanisms underlying EV-A71 and EV-D68 infection is paramount. Here, we summarize the components of the proteostasis network that are intercepted by EV-A71 and EV-D68, as well as antivirals that target this network and may help develop improved antiviral drugs.
蛋白质稳态网络可确保蛋白质的成功合成、折叠、运输和降解。越来越多的证据表明，该网络可维持蛋白质组的完整性，并与细胞生理学、病理学和病毒感染有关。人类肠道病毒 A71（EV-A71）和 EV-D68 被怀疑是急性弛缓性脊髓炎的病原体，这是一种类似脊髓灰质炎的严重神经系统综合征，目前尚无已知的治愈方法。在这种情况下，进一步阐明 EV-A71 和 EV-D68 感染的分子机制至关重要。在这里，我们总结了 EV-A71 和 EV-D68 感染所涉及的蛋白质稳态网络的组成部分，以及针对该网络的抗病毒药物，这些药物可能有助于开发更有效的抗病毒药物。
Zotero 插件