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.


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*


  • Antiviral Agents
  • Internal Ribosome Entry Sites