Regulation of the proteostasis network during enterovirus infection: A feedforward mechanism for EV-A71 and EV-D68

Jia Rong Jheng; Yuan Siao Chen; Jim Tong Horng

doi:10.1016/j.antiviral.2021.105019

Regulation of the proteostasis network during enterovirus infection: A feedforward mechanism for EV-A71 and EV-D68

Jia Rong Jheng
, Yuan Siao Chen
, Jim Tong Horng^*

^*Corresponding author for this work

Department of Biochemistry

Research output: Contribution to journal › Review article › peer-review

4 Scopus citations

Abstract

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.

Original language	English
Article number	105019
Journal	Antiviral Research
Volume	188
DOIs	https://doi.org/10.1016/j.antiviral.2021.105019
State	Published - 04 2021

Bibliographical note

Publisher Copyright:
© 2021

Keywords

Antiviral
ER stress
Enterovirus A71
Enterovirus D68
Proteostasis network
Unfolded protein response

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10.1016/j.antiviral.2021.105019

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title = "Regulation of the proteostasis network during enterovirus infection: A feedforward mechanism for EV-A71 and EV-D68",

abstract = "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.",

keywords = "Antiviral, ER stress, Enterovirus A71, Enterovirus D68, Proteostasis network, Unfolded protein response",

author = "Jheng, \{Jia Rong\} and Chen, \{Yuan Siao\} and Horng, \{Jim Tong\}",

note = "Publisher Copyright: {\textcopyright} 2021",

year = "2021",

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doi = "10.1016/j.antiviral.2021.105019",

language = "英语",

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journal = "Antiviral Research",

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AU - Chen, Yuan Siao

AU - Horng, Jim Tong

PY - 2021/4

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AB - 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.

KW - Antiviral

KW - ER stress

KW - Enterovirus A71

KW - Enterovirus D68

KW - Proteostasis network

KW - Unfolded protein response

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DO - 10.1016/j.antiviral.2021.105019

M3 - 文献综述

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AN - SCOPUS:85101389625

SN - 0166-3542

VL - 188

JO - Antiviral Research

JF - Antiviral Research

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ER -

Regulation of the proteostasis network during enterovirus infection: A feedforward mechanism for EV-A71 and EV-D68

Abstract

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Keywords

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