ArticlePLoS pathogens2017
Enterovirus 71 protease 2Apro and 3Cpro differentially inhibit the cellular endoplasmic reticulum-associated degradation (ERAD) pathway via distinct mechanisms, and enterovirus 71 hijacks ERAD component p97 to promote its replication.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Targeting Picornavirus Nonstructural 2C Protein: Structure, Function, and Antiviral Discovery.ACS infectious diseases · 2026Review
- Gene Therapy with Enterovirus 3 C Protease: A Promising Strategy for Various Solid Tumors.Nature communications · 2025Article
- ZYG11B suppresses multiple enteroviruses by triggering viral VP1 degradation.Journal of virology · 2025Article
- Selenoprotein K at the intersection of cellular pathways.Archives of biochemistry and biophysics · 2025Review
- ATPase Valosin-Containing Protein (VCP) Is Involved During the Replication and Egress of Sialodacryoadenitis Virus (SDAV) in Neurons.International journal of molecular sciences · 2024Article
- The EV71 2A protease occupies the central cleft of SETD3 and disrupts SETD3-actin interaction.Nature communications · 2024Article
- Picornavirus 2C proteins: structure-function relationships and interactions with host factors.Frontiers in cellular and infection microbiology · 2024Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Article
- How host ER membrane chaperones and morphogenic proteins support virus infection.Journal of cell science · 2023Article
- Selenoprotein S Interacts with the Replication and Transcription Complex of SARS-CoV-2 by Binding nsp7.Journal of molecular biology · 2023Article
- Current status of hand-foot-and-mouth disease.Journal of biomedical science · 2023Review
- Selenoprotein S: A versatile disordered protein.Archives of biochemistry and biophysics · 2022Review
- How Viruses Use the VCP/p97 ATPase Molecular Machine.Viruses · 2021Review
- Embryotoxic activity of 3C protease of human hepatitis A virus in developing Danio rerio embryos.Scientific reports · 2021Article
- Article
- TAR DNA-Binding Protein 43 is Cleaved by the Protease 3C of Enterovirus A71.Virologica Sinica · 2021Article
- Enterovirus 71 Induces INF2 Cleavage via Activated Caspase-2 in Infected RD Cells.Frontiers in microbiology · 2021Article
- Dysregulated autophagy contributes to the pathogenesis of enterovirus A71 infection.Cell & bioscience · 2020Review
- The Function and Mechanism of Enterovirus 71 (EV71) 3C Protease.Current microbiology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum-associated degradation (ERAD) is an important function for cellular homeostasis. The mechanism of how picornavirus infection interferes with ERAD remains unclear. In this study, we demonstrated that enterovirus 71 (EV71) infection significantly inhibits cellular ERAD by targeting multiple key ERAD molecules with its proteases 2Apro and 3Cpro using different mechanisms. Ubc6e was identified as the key E2 ubiquitin-conjugating enzyme in EV71 disturbed ERAD. EV71 3Cpro cleaves Ubc6e at Q219G, Q260S, and Q273G. EV71 2Apro mainly inhibits the de novo synthesis of key ERAD molecules Herp and VIMP at the protein translational level. Herp differentially participates in the degradation of different glycosylated ERAD substrates α-1 antitrypsin Null Hong Kong (NHK) and the C-terminus of sonic hedgehog (SHH-C) via unknown mechanisms. p97 was identified as a host factor in EV71 replication; it redistributed and co-exists with the viral protein and other known replication-related molecules in EV71-induced replication organelles. Electron microscopy and multiple-color confocal assays also showed that EV71-induced membranous vesicles were closely associated with the endoplasmic reticulum (ER), and the ER membrane molecule RTN3 was redistributed to the viral replication complex during EV71 infection. Therefore, we propose that EV71 rearranges ER membranes and hijacks p97 from cellular ERAD to benefit its replication. These findings add to our understanding of how viruses disturb ERAD and provide potential anti-viral targets for EV71 infection.
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Registered trials
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