ArticleArchives of virology2018
Suppression of the toll-like receptor 7-dependent type I interferon production pathway by autophagy resulting from enterovirus 71 and coxsackievirus A16 infections facilitates their replication.
Article in Archives of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Role of autophagy in antiviral innate immunity.Cellular & molecular biology letters · 2026Review
- Review
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Review
- The uncoating of EV71 in mature late endosomes requires CD-M6PR.Biology open · 2022Article
- Autophagy Modulators in Coronavirus Diseases: A Double Strike in Viral Burden and Inflammation.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Studies Progression on the Function of Autophagy in Viral Infection.Frontiers in cell and developmental biology · 2021Review
- Review
- Dysregulated autophagy contributes to the pathogenesis of enterovirus A71 infection.Cell & bioscience · 2020Review
- Cell Clearing Systems as Targets of Polyphenols in Viral Infections: Potential Implications for COVID-19 Pathogenesis.Antioxidants (Basel, Switzerland) · 2020Review
- Regulation of Innate Immune Responses by Autophagy: A Goldmine for Viruses.Frontiers in immunology · 2020Review
- Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus InfectionFrontiers in cellular and infection microbiology · 2020Article
- Molecular Pathogenicity of Enteroviruses Causing Neurological Disease.Frontiers in microbiology · 2020Review
- Interplays between Enterovirus A71 and the innate immune system.Journal of biomedical science · 2019Review
- The Intertwined Life Cycles of Enterovirus and Autophagy.Virulence · 2019Review
- Review
- Crosstalk between Autophagy and Type I Interferon Responses in Innate Antiviral Immunity.Viruses · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) act as molecular sentinels, detecting invading viral pathogens and triggering host innate immune responses, including autophagy. However, many viruses have evolved a series of strategies to manipulate autophagy for their own benefit. Enterovirus 71 (EV71) and coxsackievirus A16 (CA16), as the primary agents causing hand, foot and mouth disease (HFMD), can induce autophagy leading to their replication. Therefore, the objective of this study was to investigate whether enhanced viral replication caused by autophagy in EV71 and CA16 infections was associated with a TLR-related signaling pathway. Our results demonstrate that complete autophagy and incomplete autophagy were observed in human bronchial epithelial (16HBE) cells infected with EV71 and CA16. Moreover, suppression of autophagy by the pharmacological modulator 3-MA significantly and clearly decreased the survival rates and viral replication of EV71 and CA16 in 16HBE cells. Inhibition of autophagy also enhanced the expression of molecules related to the TLR7-dependent type I interferon (IFN-I) production pathway, such as TLR7, MyD88, IRF7 and IFN-α/β. Finally, immunofluorescence staining demonstrated that TLR7 endosome marker M6PR levels were clearly reduced in EV71- and CA16-infected cells, while they were markedly elevated in infected cells treated with 3-MA. These findings suggest that increased EV71 and CA16 replication meditated by autophagy in 16HBE cells might promote degradation of the endosome, leading to suppression of the TLR7-mediated IFN-I signaling pathway.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.