ArticleJournal of virology2014
Enterovirus 68 3C protease cleaves TRIF to attenuate antiviral responses mediated by Toll-like receptor 3.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 75 citations in OpenAlex.
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- ARRDC3 promotes lysosome-mediated YAP degradation to inhibit enterovirus replication.Virologica Sinica · 2025Article
- Combined Antiviral and Cytoprotective Action of Rosmarinic Acid Against EV-A71 Infection: A Potential Therapeutic Strategy.Pathogens (Basel, Switzerland) · 2025Article
- Cullin 3-mediated ubiquitination restricts enterovirus D68 replication and is counteracted by viral protease 3C.Journal of virology · 2025Article
- The structural protein VP3 of enterovirus D68 interacts with MAVS to inhibit the NF-κB signaling pathway.Journal of virology · 2025Article
- Insights Into Enterovirus D68 Immunology: Unraveling the Mysteries of Host-Pathogen Interactions.Immunity, inflammation and disease · 2025Review
- Enteroviral 3C protease cleaves N4BP1 to impair the host inflammatory response.Journal of virology · 2025Article
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- Antiviral immunity within neural stem cells distinguishes Enterovirus-D68 strain differences in forebrain organoids.Journal of neuroinflammation · 2024Article
- Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1.Journal of virology · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- The Picornaviridae Family: Knowledge Gaps, Animal Models, Countermeasures, and Prototype Pathogens.The Journal of infectious diseases · 2023Article
- Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host.Virologica Sinica · 2023Article
- CD74 Interacts with Proteins of Enterovirus D68 To Inhibit Virus Replication.Microbiology spectrum · 2023Article
- Enterovirus D68 VP3 Targets the Interferon Regulatory Factor 7 To Inhibit Type I Interferon Response.Microbiology spectrum · 2023Article
- Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Enterovirus 3C Protease Cleaves TRIM7 To Dampen Its Antiviral Activity.Journal of virology · 2022Article
- Animal Models of Enterovirus D68 Infection and Disease.Journal of virology · 2022Review
- Surgical Strikes on Host Defenses: Role of the Viral Protease Activity in Innate Immune Antagonism.Pathogens (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
unlabelledHuman enterovirus 68 (EV68) is a member of the EV-D species, which belongs to the EV genus of the Picornaviridae family. Over the past several years, there have been increasingly documented outbreaks of respiratory disease associated with EV68. As a globally emerging pathogen, EV68 infects both adults and children. However, the molecular basis of EV68 pathogenesis is unknown. Here we report that EV68 inhibits Toll-like receptor 3 (TLR3)-mediated innate immune responses by targeting the TIR domain-containing adaptor inducing beta interferon (TRIF). In infected HeLa cells, EV68 inhibits poly(I·C)-induced interferon regulatory factor 3 (IRF3) activation and beta interferon (IFN-β) expression. Further investigations revealed that TRIF, a critical adaptor downstream of TLR3, is targeted by EV68. When expressed alone, 3C(pro), an EV68-encoded protease, cleaves TRIF. 3C(pro) mediates TRIF cleavage at Q312 and Q653, which are sites in the amino- and carboxyl-terminal domains, respectively. This cleavage relies on 3C(pro)'s cysteine protease activity. Cleavage of TRIF abolishes the capacity of TRIF to activate NF-κB and IFN-β signaling. These results suggest that control of TRIF by 3C(pro) may be a mechanism by which EV68 subverts host innate immune responses. IMPORTANCE: EV68 is a globally emerging pathogen, but the molecular basis of EV68 pathogenesis is unclear. Here we report that EV68 inhibits TLR3-mediated innate immune responses by targeting TRIF. Further investigations revealed that TRIF is cleaved by 3C(pro). These results suggest that control of TRIF by 3C(pro) may be a mechanism by which EV68 impairs type I IFN production in response to TLR3 activation.
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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.