ArticleJournal of virology2007
Mouse hepatitis coronavirus A59 nucleocapsid protein is a type I interferon antagonist.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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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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Who cites it
86 citing papers in PubMed, 109 citations in OpenAlex.
- Article
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- Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective.The EMBO journal · 2024Review
- The Nucleocapsid Proteins of SARS-CoV-2 and Its Close Relative Bat Coronavirus RaTG13 Are Capable of Inhibiting PKR- and RNase L-Mediated Antiviral Pathways.Microbiology spectrum · 2023Article
- Attenuated Viral Replication of AvianMicrobiology spectrum · 2022Article
- Antagonism of Protein Kinase R by Large DNA Viruses.Pathogens (Basel, Switzerland) · 2022Review
- Porcine epidemic diarrhea virus strain FJzz1 infection induces type I/III IFNs production through RLRs and TLRs-mediated signaling.Frontiers in immunology · 2022Article
- The Role of Coronavirus RNA-Processing Enzymes in Innate Immune Evasion.Life (Basel, Switzerland) · 2021Review
- Low type I interferon response in COVID-19 patients: Interferon response may be a potential treatment for COVID-19.Biomedical reports · 2021Article
- SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial-derived cells and cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
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- Murine-β-coronavirus-induced neuropathogenesis sheds light on CNS pathobiology of SARS-CoV2.Journal of neurovirology · 2021Review
- Possible Therapeutic Intervention Strategies for COVID-19 by Manipulating the Cellular Proteostasis Network.Advances in experimental medicine and biology · 2021Article
- Coronaviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines.Trends in immunology · 2020Review
- Porcine Epidemic Diarrhea Virus and the Host Innate Immune Response.Pathogens (Basel, Switzerland) · 2020Review
- Porcine deltacoronavirus nucleocapsid protein antagonizes IFN-β production by impairing dsRNA and PACT binding to RIG-I.Virus genes · 2019Article
- The crystal structure of main protease from mouse hepatitis virus A59 in complex with an inhibitor.Biochemical and biophysical research communications · 2019Article
- PEDV and PDCoV Pathogenesis: The Interplay Between Host Innate Immune Responses and Porcine Enteric Coronaviruses.Frontiers in veterinary science · 2019Review
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
- Nucleocapsid protein from porcine epidemic diarrhea virus isolates can antagonize interferon-λ production by blocking the nuclear factor-κB nuclear translocation.Journal of Zhejiang University. Science. B · 2018Article
26 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
5 authors at 1 institution in 1 country.
Funding
Abstract
The recent emergence of several new coronaviruses, including the etiological cause of severe acute respiratory syndrome, has significantly increased the importance of understanding virus-host cell interactions of this virus family. We used mouse hepatitis virus (MHV) A59 as a model to gain insight into how coronaviruses affect the type I alpha/beta interferon (IFN) system. We demonstrate that MHV is resistant to type I IFN. Protein kinase R (PKR) and the alpha subunit of eukaryotic translation initiation factor are not phosphorylated in infected cells. The RNase L activity associated with 2',5'-oligoadenylate synthetase is not activated or is blocked, since cellular RNA is not degraded. These results are consistent with lack of protein translation shutoff early following infection. We used a well-established recombinant vaccinia virus (VV)-based expression system that lacks the viral IFN antagonist E3L to screen viral genes for their ability to rescue the IFN sensitivity of the mutant. The nucleocapsid (N) gene rescued VVDeltaE3L from IFN sensitivity. N gene expression prevents cellular RNA degradation and partially rescues the dramatic translation shutoff characteristic of the VVDeltaE3L virus. However, it does not prevent PKR phosphorylation. The results indicate that the MHV N protein is a type I IFN antagonist that likely plays a role in circumventing the innate immune response.
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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.