ArticleJournal of virology2016
3C Protease of Enterovirus D68 Inhibits Cellular Defense Mediated by Interferon Regulatory Factor 7.
Article in Journal of virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 71 citations in OpenAlex.
- Enterovirus infections in children.Pediatric investigation · 2026Review
- Respiratory enterovirus D68: virology, clinical surveillance, host-pathogen interactions, and therapeutic prospects.Frontiers in cellular and infection microbiology · 2026Review
- Review
- 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
- Enterovirus D68 infection in cotton rats results in systemic inflammation with detectable viremia associated with extracellular vesicle and neurologic disease.Scientific reports · 2025Article
- Insights Into Enterovirus D68 Immunology: Unraveling the Mysteries of Host-Pathogen Interactions.Immunity, inflammation and disease · 2025Review
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1.Journal of virology · 2024Article
- Understanding the Neurotrophic Virus Mechanisms and Their Potential Effect on Systemic Lupus Erythematosus Development.Brain sciences · 2024Review
- The impact of genetically controlled splicing on exon inclusion and protein structure.PloS one · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Mass spectrometric assays monitoring the deubiquitinase activity of the SARS-CoV-2 papain-like protease inform on the basis of substrate selectivity and have utility for substrate identification.Bioorganic & medicinal chemistry · 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
- Pathogenesis of enterovirus infection in central nervous system.Biosafety and health · 2023Review
- Enterovirus D68 VP3 Targets the Interferon Regulatory Factor 7 To Inhibit Type I Interferon Response.Microbiology spectrum · 2023Article
- Mitochondria Dysfunction at the Heart of Viral Myocarditis: Mechanistic Insights and Therapeutic Implications.Viruses · 2023Review
- Pterostilbene, an active constituent of blueberries, enhances innate immune activation and restricts enterovirus D68 infection.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
unlabelledHuman enterovirus 68 (EV-D68) is a member of the EV-D species, which belongs to the EV genus of the Picornaviridae family. Over the past several years, clusters of EV-D68 infections have occurred worldwide. A recent outbreak in the United States is the largest one associated with severe respiratory illness and neurological complication. Although clinical symptoms are recognized, the virus remains poorly understood. Here we report that EV-D68 inhibits innate antiviral immunity by downregulation of interferon regulatory factor 7 (IRF7), an immune factor with a pivotal role in viral pathogenesis. This process depends on 3C(pro), an EV-D68-encoded protease, to mediate IRF7 cleavage. When expressed in host cells, 3C(pro) targets Q167 and Q189 within the constitutive activation domain, resulting in cleavage of IRF7. Accordingly, wild-type IRF7 is fully active. However, IRF7 cleavage abrogated its capacity to activate type I interferon expression and limit replication of EV-D68. Notably, IRF7 cleavage strictly requires the protease activity of 3C(pro). Together, these results suggest that a dynamic interplay between 3C(pro) and IRF7 may determine the outcome of EV-D68 infection. IMPORTANCE: EV-D68 is a globally emerging pathogen, but the molecular basis of EV-D68 pathogenesis is unclear. Here we report that EV-D68 inhibits innate immune responses by targeting an immune factor, IRF7. This involves the 3C protease encoded by EV-D68, which mediates the cleavage of IRF7. These observations suggest that the 3C(pro)-IRF7 interaction may represent an interface that dictates EV-D68 infection.
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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.