ArticleJournal of virology2009
Classical swine fever virus can remain virulent after specific elimination of the interferon regulatory factor 3-degrading function of Npro.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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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.
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Who cites it
35 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- New Generation Self-Replicating RNA Vaccines Derived from Pestivirus Genome.Methods in molecular biology (Clifton, N.J.) · 2024Article
- N-terminal domain of classical swine fever virus NJournal of virology · 2023Article
- A Genetically Engineered Bivalent Vaccine Coexpressing a Molecular Adjuvant against Classical Swine Fever and Porcine Epidemic Diarrhea.International journal of molecular sciences · 2023Article
- Pestiviruses infection: Interferon-virus mutual regulation.Frontiers in cellular and infection microbiology · 2023Review
- Immunoinformatic prediction of the pathogenicity of bovine viral diarrhea virus genotypes: implications for viral virulence determinants, designing novel diagnostic assays and vaccines development.Frontiers in veterinary science · 2023Article
- Removal of the EJournal of virology · 2022Article
- HSP90AA1 interacts with CSFV NS5A protein and regulates CSFV replicationFrontiers in immunology · 2022Article
- Disruption of interferon-β production by the NVirulence · 2021Article
- Characteristics of Classical Swine Fever Virus Variants Derived from Live Attenuated GPEViruses · 2021Article
- 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
- Review
- Apoptosis, Autophagy, and Pyroptosis: Immune Escape Strategies for Persistent Infection and Pathogenesis of Classical Swine Fever Virus.Pathogens (Basel, Switzerland) · 2019Review
- Article
- Pestivirus Npro Directly Interacts with Interferon Regulatory Factor 3 Monomer and Dimer.Journal of virology · 2016Article
- PKR activation enhances replication of classical swine fever virus in PK-15 cells.Virus research · 2015Article
- Analysis of a pair of END+ and END- viruses derived from the same bovine viral diarrhea virus stock reveals the amino acid determinants in Npro responsible for inhibition of type I interferon production.The Journal of veterinary medical science · 2015Article
- Lipid Binding of the Amphipathic Helix Serving as Membrane Anchor of Pestivirus Glycoprotein Erns.PloS one · 2015Article
- Postnatal persistent infection with classical Swine Fever virus and its immunological implications.PloS one · 2015Article
- Immune Responses Against Classical Swine Fever Virus: Between Ignorance and Lunacy.Frontiers in veterinary science · 2015Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pestiviruses prevent alpha/beta interferon (IFN-alpha/beta) production by promoting proteasomal degradation of interferon regulatory factor 3 (IRF3) by means of the viral N(pro) nonstructural protein. N(pro) is also an autoprotease, and its amino-terminal coding sequence is involved in translation initiation. We previously showed with classical swine fever virus (CSFV) that deletion of the entire N(pro) gene resulted in attenuation in pigs. In order to elaborate on the role of the N(pro)-mediated IRF3 degradation in classical swine fever pathogenesis, we searched for minimal amino acid substitutions in N(pro) that would specifically abrogate this function. Our mutational analyses showed that degradation of IRF3 and autoprotease activity are two independent but structurally overlapping functions of N(pro). We describe two mutations in N(pro) that eliminate N(pro)-mediated IRF3 degradation without affecting the autoprotease activity. We also show that the conserved standard sequence at these particular positions is essential for N(pro) to interact with IRF3. Surprisingly, when these two mutations are introduced independently in the backbones of highly and moderately virulent CSFV, the resulting viruses are not attenuated, or are only partially attenuated, in 8- to 10-week-old pigs. This contrasts with the fact that these mutant viruses have lost the capacity to degrade IRF3 and to prevent IFN-alpha/beta induction in porcine cell lines and monocyte-derived dendritic cells. Taken together, these results demonstrate that contrary to previous assumptions and to the case for other viral systems, impairment of IRF3-dependent IFN-alpha/beta induction is not a prerequisite for CSFV virulence.
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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.