ArticleJournal of virology2018
A Single Amino Acid Substitution within the Paramyxovirus Sendai Virus Nucleoprotein Is a Critical Determinant for Production of Interferon-Beta-Inducing Copyback-Type Defective Interfering Genomes.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Structural insights into measles virus RNA synthesis regulation and pan-paramyxoviral polymerase inhibition by ERDRP-0519.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Variable and conserved features of copy-back viral genome populations generatedJournal of virology · 2026Article
- Mumps Virus: Replication, Immune Response, and the Changing Landscape of Vaccine Effectiveness.Pathogens (Basel, Switzerland) · 2026Review
- Discovery of a pre-vein progenitor that requires VEGF/ERK inhibition to complete vein differentiation.bioRxiv : the preprint server for biology · 2025Article
- Nano-Flow Cytometry-Guided Discrimination and Separation of Human Cytomegalovirus Virions and Extracellular Vesicles.Journal of extracellular vesicles · 2025Article
- Role of Defective Interfering Particles in Complement-Mediated Lysis of Parainfluenza Virus-Infected Cells.Viruses · 2025Article
- Antivirotics based on defective interfering particles: emerging concepts and challenges.Frontiers in cellular and infection microbiology · 2025Review
- Review
- Single-cell transcriptome analysis illuminating the characteristics of species-specific innate immune responses against viral infections.GigaScience · 2023Article
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- The Role of Nucleoprotein in Immunity to Human Negative-Stranded RNA Viruses-Not Just Another Brick in the Viral Nucleocapsid.Viruses · 2022Review
- Population Variability Generated during Rescue Process and Passaging of Recombinant Mumps Viruses.Viruses · 2021Article
- Identification and Characterization of Defective Viral Genomes in Ebola Virus-Infected Rhesus Macaques.Journal of virology · 2021Article
- Sarbecovirus ORF6 proteins hamper induction of interferon signaling.Cell reports · 2021Article
- SARS-CoV-2 ORF3b Is a Potent Interferon Antagonist Whose Activity Is Increased by a Naturally Occurring Elongation Variant.Cell reports · 2020Article
- Defective Interfering Particles of Negative-Strand RNA Viruses.Trends in microbiology · 2020Review
- Viral evolution identifies a regulatory interface between paramyxovirus polymerase complex and nucleocapsid that controls replication dynamics.Science advances · 2020Article
- Porcine Deltacoronavirus Accessory Protein NS7a Antagonizes IFN-β Production by Competing With TRAF3 and IRF3 for Binding to IKKε.Frontiers in cellular and infection microbiology · 2020Article
- Defective viral genomes are key drivers of the virus-host interaction.Nature microbiology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the first defenses against infecting pathogens is the innate immune system activated by cellular recognition of pathogen-associated molecular patterns (PAMPs). Although virus-derived RNA species, especially copyback (cb)-type defective interfering (DI) genomes, have been shown to serve as real PAMPs, which strongly induce interferon-beta (IFN-β) during mononegavirus infection, the mechanisms underlying DI generation remain unclear. Here, for the first time, we identified a single amino acid substitution causing production of cbDI genomes by successful isolation of two distinct types of viral clones with cbDI-producing and cbDI-nonproducing phenotypes from the stock Sendai virus (SeV) strain Cantell, which has been widely used in a number of studies on antiviral innate immunity as a representative IFN-β-inducing virus. IFN-β induction was totally dependent on the presence of a significant amount of cbDI genome-containing viral particles (DI particles) in the viral stock, but not on deficiency of the IFN-antagonistic viral accessory proteins C and V. Comparison of the isolates indicated that a single amino acid substitution found within the N protein of the cbDI-producing clone was enough to cause the emergence of DI genomes. The mutated N protein of the cbDI-producing clone resulted in a lower density of nucleocapsids than that of the DI-nonproducing clone, probably causing both production of the DI genomes and their formation of a stem-loop structure, which serves as an ideal ligand for RIG-I. These results suggested that the integrity of mononegaviral nucleocapsids might be a critical factor in avoiding the undesirable recognition of infection by host cells.
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