ArticleJournal of virology2011
Classical swine fever virus N(pro) limits type I interferon induction in plasmacytoid dendritic cells by interacting with interferon regulatory factor 7.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 93 citations in OpenAlex.
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- Detection of Phocoena Pestivirus and Neutralizing Antibodies in Harbor Porpoises Found Dead at the North Sea and Baltic Sea Coasts.Transboundary and emerging diseases · 2026Article
- Strategies of Classical Swine Fever Immune Evasion.International journal of molecular sciences · 2025Review
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- N-terminal domain of classical swine fever virus NJournal of virology · 2023Article
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- IRF7: role and regulation in immunity and autoimmunity.Frontiers in immunology · 2023Review
- Current progress on innate immune evasion mediated by NFrontiers in immunology · 2023Review
- Pestiviruses infection: Interferon-virus mutual regulation.Frontiers in cellular and infection microbiology · 2023Review
- Transcriptome analysis of PK-15 cells expressing CSFV NS4A.BMC veterinary research · 2022Article
- Cholesterol Biosynthesis Modulates CSFV Replication.Viruses · 2022Article
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- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- Activation of Dendritic Cells in Tonsils Is Associated with CD8 T Cell Responses following Vaccination with Live Attenuated Classical Swine Fever Virus.International journal of molecular sciences · 2021Article
- The EViruses · 2021Article
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- Isolation and Characterization of Porcine Astrovirus 5 from a Classical Swine Fever Virus-Infected Specimen.Journal of virology · 2020Article
- High-Resolution Profiling of Innate Immune Responses by Porcine Dendritic Cell SubsetsFrontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses are detected by different classes of pattern recognition receptors that lead to the activation of interferon regulatory factors (IRF) and consequently to the induction of alpha/beta interferon (IFN-α/β). In turn, efficient viral strategies to escape the type I IFN-induced antiviral mechanisms have evolved. Previous studies established that pestivirus N(pro) antagonizes the early innate immune response by targeting the transcription factor IRF3 for proteasomal degradation. Here, we report that N(pro) of classical swine fever virus (CSFV) interacts also with IRF7, another mediator of type I IFN induction. We demonstrate that the Zn-binding domain of N(pro) is essential for the interaction of N(pro) with IRF7. For IRF3 and IRF7, the DNA-binding domain, the central region, and most of the regulatory domain are required for the interaction with N(pro). Importantly, the induction of IRF7-dependent type I IFN responses in plasmacytoid dendritic cells (pDC) is reduced after wild-type CSFV infection compared with infection with virus mutants unable to interact with IRF7. This is associated with lower levels of IRF7 in pDC. Consequently, wild-type but not N(pro) mutant CSFV-infected pDC show reduced responses to other stimuli. Taken together, the results of this study show that CSFV N(pro) is capable of manipulating the function of IRF7 in pDC and provides the virus with an additional strategy to circumvent the innate defense.
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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.