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

Antiviral Res. 2021 Apr:188:105019. doi: 10.1016/j.antiviral.2021.105019. Epub 2021 Jan 20.

Authors

Jia-Rong Jheng¹, Yuan-Siao Chen¹, Jim-Tong Horng²

Affiliations

¹ Department of Biochemistry and Molecular Biology, College of Medicine, Chang Gung University, Kweishan, Taoyuan, Taiwan.
² 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. Electronic address: jimtong@mail.cgu.edu.tw.

PMID: 33484748
DOI: 10.1016/j.antiviral.2021.105019

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.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Antiviral Agents / pharmacology
Antiviral Agents / therapeutic use
Endoplasmic Reticulum / metabolism
Enterovirus A, Human / genetics
Enterovirus A, Human / physiology*
Enterovirus D, Human / genetics
Enterovirus D, Human / physiology*
Enterovirus Infections / drug therapy
Enterovirus Infections / virology
Humans
Internal Ribosome Entry Sites
Protein Biosynthesis
Proteolysis
Proteostasis*

Substances

Antiviral Agents
Internal Ribosome Entry Sites