ArticleJournal of virology2014
Hepatitis A virus 3C protease cleaves NEMO to impair induction of beta interferon.
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 64 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
64 citing papers in PubMed, 87 citations in OpenAlex.
- Host species-specific mutations in the thumb domain of the 3Dpol polymerase are required for efficient replication of human hepatitis A virus in mice.PLoS pathogens · 2026Article
- SADS-CoV nsp5 Inhibits Interferon Production by Targeting Kinase IKKε.Microorganisms · 2025Article
- Redefining the immune landscape of hepatitis A virus infection.Experimental & molecular medicine · 2025Review
- Limited impact of hepatitis A virus 3C protease-mediated cleavage on the functions of NEMO in human hepatocytes.Journal of virology · 2025Article
- HCoV-229E Mpro Suppresses RLR-Mediated Innate Immune Signalling Through Cleavage of NEMO and Through Other Mechanisms.International journal of molecular sciences · 2025Article
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- Viral protease cleavage of MAVS in genetically modified mice with hepatitis A virus infection.Journal of hepatology · 2023Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Review
- SARS-CoV-2 nsp5 Exhibits Stronger Catalytic Activity and Interferon Antagonism than Its SARS-CoV Ortholog.Journal of virology · 2022Article
- High-Content Screening and Computational Prediction Reveal Viral Genes That Suppress the Innate Immune Response.mSystems · 2022Article
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- Porcine Sapelovirus 3CFrontiers in cellular and infection microbiology · 2022Article
- Modulation of Innate Antiviral Immune Response by Porcine Enteric Coronavirus.Frontiers in microbiology · 2022Review
- Luciferase-Based Biosensors in the Era of the COVID-19 Pandemic.ACS nanoscience Au · 2021Review
- Pathogenicity and virulence of hepatitis A virus.Virulence · 2021Review
- Degradation of Host Proteins and Apoptosis Induced by Foot-and-Mouth Disease Virus 3C Protease.Pathogens (Basel, Switzerland) · 2021Article
- The NF-κB Transcriptional Footprint Is Essential for SARS-CoV-2 Replication.Journal of virology · 2021Article
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- Prolonged Gut Dysbiosis and Fecal Excretion of Hepatitis A Virus in Patients Infected with Human Immunodeficiency Virus.Viruses · 2021Observational
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
NEMO (NF-κB essential modulator) is a bridging adaptor indispensable for viral activation of interferon (IFN) antiviral response. Herein, we show that hepatitis A virus (HAV) 3C protease (3Cpro) cleaves NEMO at the Q304 residue, negating its signaling adaptor function and abrogating viral induction of IFN-β synthesis via the retinoic acid-inducible gene I/melanoma differentiation-associated protein 5 (RIG-I/MDA5) and Toll-like receptor 3 (TLR3) pathways. NEMO cleavage and IFN antagonism, however, were lost upon ablation of the catalytic activity of 3Cpro. These data describe a novel immune evasion mechanism of HAV.
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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.