ArticleJournal of virology2020
Middle East Respiratory Syndrome Coronavirus Nucleocapsid Protein Suppresses Type I and Type III Interferon Induction by Targeting RIG-I Signaling.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 91 citations in OpenAlex.
- Viral Mechanisms and Drug Influences on Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) Pathway in Human Coronaviruses Infection: A Systematic Review.Health science reports · 2026Review
- A new approach to discovering a broad-spectrum anti-respiratory virus drug: Tubeimoside II modulates host factor PACT to potentiate the RIG-I antiviral pathway.Acta pharmaceutica Sinica. B · 2026Article
- Detection and host associations of Nairobi sheep disease virus in the human upper respiratory tract in Beijing, China.Frontiers in microbiology · 2026Article
- A Narrative Review on the Recent Insights Into the Pathogenicity and Potential Role of Middle East Respiratory Syndrome Coronavirus (MERS-CoV) in the Emergence of "Disease X".Health science reports · 2025Article
- SADS-CoV nsp5 Inhibits Interferon Production by Targeting Kinase IKKε.Microorganisms · 2025Article
- Betacoronavirus internal protein: role in immune evasion and viral pathogenesis.Journal of virology · 2025Review
- The R203M and D377Y mutations of the nucleocapsid protein promote SARS-CoV-2 infectivity by impairing RIG-I-mediated antiviral signaling.PLoS pathogens · 2025Article
- Recent Advances of Type I Interferon on the Regulation of Immune Cells and the Treatment of Systemic Lupus Erythematosus.Journal of inflammation research · 2025Review
- Intestinal-pulmonary axis: a 'Force For Good' against respiratory viral infections.Frontiers in immunology · 2025Review
- Intrinsic factors behind long COVID: exploring the role of nucleocapsid protein in thrombosis.PeerJ · 2025Review
- Coronavirus nucleocapsid proteins: a multifaceted modulator in the innate immune evasion.Frontiers in microbiology · 2025Review
- Characteristics and mechanisms of liver injury caused by emerging infectious diseases.Frontiers in immunology · 2025Review
- Viral strategies to antagonize the host antiviral innate immunity: an indispensable research direction for emerging virus-host interactions.Emerging microbes & infections · 2024Review
- MERS-CoV-nsp5 expression in human epithelial BEAS 2b cells attenuates type I interferon production by inhibiting IRF3 nuclear translocation.Cellular and molecular life sciences : CMLS · 2024Article
- Swine acute diarrhea syndrome coronavirus nucleocapsid protein antagonizes the IFN response through inhibiting TRIM25 oligomerization and functional activation of RIG-I/TRIM25.Veterinary research · 2024Article
- Retinoic Acid-Mediated Inhibition of Mouse Coronavirus Replication Is Dependent on IRF3 and CaMKK.Viruses · 2024Article
- Structural proteins of human coronaviruses: what makes them different?Frontiers in cellular and infection microbiology · 2024Review
- Interaction between coronaviruses and the autophagic response.Frontiers in cellular and infection microbiology · 2024Review
- Exploring TRIM proteins' role in antiviral defense against influenza A virus and respiratory coronaviruses.Frontiers in cellular and infection microbiology · 2024Review
- Genetic diversity and molecular epidemiology of Middle East Respiratory Syndrome Coronavirus in dromedaries in Ethiopia, 2017-2020.Emerging microbes & infections · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I and type III interferons (IFNs) are the frontline of antiviral defense mechanisms that trigger hundreds of downstream antiviral genes. In this study, we observed that MERS-CoV nucleocapsid (N) protein suppresses type I and type III IFN gene expression. The N protein suppresses Sendai virus-induced IFN-β and IFN-λ1 by reducing their promoter activity and mRNA levels, as well as downstream IFN-stimulated genes (ISGs). Retinoic acid-inducible gene I (RIG-I) is known to recognize viral RNA and induce IFN expression through tripartite motif-containing protein 25 (TRIM25)-mediated ubiquitination of RIG-I caspase activation and recruitment domains (CARDs). We discovered that MERS-CoV N protein suppresses RIG-I-CARD-induced, but not MDA5-CARD-induced, IFN-β and IFN-λ1 promoter activity. By interacting with TRIM25, N protein impedes RIG-I ubiquitination and activation and inhibits the phosphorylation of transcription factors IFN-regulatory factor 3 (IRF3) and NF-κB that are known to be important for IFN gene activation. By employing a recombinant Sindbis virus-EGFP replication system, we showed that viral N protein downregulated the production of not only IFN mRNA but also bioactive IFN proteins. Taken together, MERS-CoV N protein functions as an IFN antagonist. It suppresses RIG-I-induced type I and type III IFN production by interfering with TRIM25-mediated RIG-I ubiquitination. Our study sheds light on the pathogenic mechanism of how MERS-CoV causes disease.
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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.