ArticleEmerging microbes & infections2016
Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3.
Article in Emerging microbes & infections, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 132 citations in OpenAlex.
- Modulation of Host Innate Immune Response by Highly Pathogenic Human Coronaviruses during Viral Infection.Journal of microbiology and biotechnology · 2026Review
- The structure and function of membrane protein in coronavirus infection and its applications in the development of vaccines and therapeutic drugs.Frontiers in microbiology · 2026Review
- Porcine Deltacoronavirus Nsp13 Suppresses the Assembly of the MAVS-TBK1-IRF3 Complex and IRF9 Nuclear Translocation.Transboundary and emerging diseases · 2026Article
- PEDV Structural Proteins with Emphasis on M Protein as an Immunomodulatory Factor in Porcine Innate Immunity.Life (Basel, Switzerland) · 2025Review
- How Does Porcine Epidemic Diarrhea Virus Escape Host Innate Immunity?Pathogens (Basel, Switzerland) · 2025Review
- Herpes simplex virus 1 encodes a STING antagonist that can be therapeutically targeted.Cell reports. Medicine · 2025Article
- Anti-interferon armamentarium of human coronaviruses.Cellular and molecular life sciences : CMLS · 2025Review
- Betacoronavirus internal protein: role in immune evasion and viral pathogenesis.Journal of virology · 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
- Exploring type I interferon pathway: virulent vs. attenuated strain of African swine fever virus revealing a novel function carried by MGF505-4R.Frontiers in immunology · 2024Article
- Structural proteins of human coronaviruses: what makes them different?Frontiers in cellular and infection microbiology · 2024Review
- The KxGxYR and DxE motifs in the C-tail of the Middle East respiratory syndrome coronavirus membrane protein are crucial for infectious virus assembly.Cellular and molecular life sciences : CMLS · 2023Article
- Insight into the mechanisms of coronaviruses evading host innate immunity.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- MERS-CoV nsp1 regulates autophagic flux via mTOR signalling and dysfunctional lysosomes.Emerging microbes & infections · 2022Article
- Article
- miR-615 facilitates porcine epidemic diarrhea virus replication by targetingFrontiers in microbiology · 2022Article
- Regulation of cGAS/STING signaling and corresponding immune escape strategies of viruses.Frontiers in cellular and infection microbiology · 2022Review
- The Robustness of Cellular Immunity Determines the Fate of SARS-CoV-2 Infection.Frontiers in immunology · 2022Review
- A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations.Frontiers in immunology · 2022Review
33 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Middle East respiratory syndrome coronavirus (MERS-CoV) infection has claimed hundreds of lives and has become a global threat since its emergence in Saudi Arabia in 2012. The ability of MERS-CoV to evade the host innate antiviral response may contribute to its severe pathogenesis. Many MERS-CoV-encoded proteins were identified to have interferon (IFN)-antagonizing properties, which correlates well with the reduced IFN levels observed in infected patients and ex vivo models. In this study, we fully characterized the IFN-antagonizing property of the MERS-CoV M protein. Expression of MERS-CoV M protein suppressed type I IFN expression in response to Sendai virus infection or poly(I:C) induction. This suppressive effect was found to be specific for the activation of IFN regulatory factor 3 (IRF3) but not nuclear factor-κB. MERS-CoV M protein interacted with TRAF3 and disrupted TRAF3-TBK1 association leading to reduced IRF3 activation. M proteins from MERS-CoV and SARS-CoV have three highly similar conserved N-terminal transmembrane domains and a C-terminal region. Using chimeric and truncation mutants, the N-terminal transmembrane domains of the MERS-CoV M protein were found to be sufficient for its inhibitory effect on IFN expression, whereas the C-terminal domain was unable to induce this suppression. Collectively, our findings suggest a common and conserved mechanism through which highly pathogenic MERS-CoV and SARS-CoV harness their M proteins to suppress type I IFN expression at the level of TBK1-dependent phosphorylation and activation of IRF3 resulting in evasion of the host innate antiviral response.
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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.