ArticleThe Journal of general virology2017
Loss of Sendai virus C protein leads to accumulation of RIG-I immunostimulatory defective interfering RNA.
Article in The Journal of general virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Concepts of RNA virus evolution for the design of better antiviral countermeasures.Nature reviews. Microbiology · 2026Review
- 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
- The human DEAD-box protein DDX3X regulates host and viral mRNA translation during Sendai Virus infection.bioRxiv : the preprint server for biology · 2026Article
- Variable and conserved features of copy-back viral genome populations generatedJournal of virology · 2026Article
- The role of M2 proteins of pneumoviruses in transcription regulation, prevention of hypermutation, and activation of the type I interferon pathway.Journal of virology · 2025Article
- Review
- Tailam paramyxovirus C protein inhibits viral replication.Journal of virology · 2024Article
- Molecular Analysis of Copy-Back Defective Interfering RNAs of Morbilliviruses.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Review
- Restriction factor screening identifies RABGAP1L-mediated disruption of endocytosis as a host antiviral defense.Cell reports · 2022Article
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- SeV C Protein Plays a Role in Restricting Macrophage Phagocytosis by Limiting the Generation of Intracellular Double-Stranded RNA.Frontiers in microbiology · 2022Article
- Article
- C Protein is Essential for Canine Distemper Virus Virulence and Pathogenicity in Ferrets.Journal of virology · 2021Article
- Virus-Intrinsic Differences and Heterogeneous IRF3 Activation Influence IFN-Independent Antiviral Protection.iScience · 2020Article
- Defective Interfering Particles of Negative-Strand RNA Viruses.Trends in microbiology · 2020Review
- Innate Intracellular Antiviral Responses Restrict the Amplification of Defective Virus Genomes of Parainfluenza Virus 5.Journal of virology · 2020Article
- Inhibition of Nipah Virus by Defective Interfering Particles.The Journal of infectious diseases · 2020Article
- The DOT1L inhibitor Pinometostat decreases the host-response against infections: Considerations about its use in human therapy.Scientific reports · 2019Article
- Defective viral genomes are key drivers of the virus-host interaction.Nature microbiology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Retinoic acid inducible gene (RIG-I)-mediated innate immunity plays a pivotal role in defence against virus infections. Previously we have shown that Sendai virus (SeV) defective interfering (DI) RNA functions as an exclusive and potent RIG-I ligand in DI-RNA-rich SeV-Cantell infected cells. To further understand how RIG-I is activated during SeV infection, we used a different interferon (IFN)-inducing SeV strain, recombinant SeVΔC, which, in contrast to SeV-Cantell is believed to stimulate IFN production due to the lack of the SeV IFN antagonist protein C. Surprisingly, we found that in SevΔC-infected cells, DI RNAs also functioned as an exclusive RIG-I ligand. Infections with wild-type SeV failed to generate any RIG-I-associated immunostimulatory RNA and this correlated with the lack of DI genomes in infected cells, as well as with the absence of cellular innate immune responses. Supplementation of the C protein in the context of SeVΔC infection led to a reduction in the number of DI RNAs, further supporting the potential role of the C protein as a negative regulator of DI generation and/or accumulation. Our findings indicate that limiting DI genome production is an important function of viral IFN antagonist proteins.
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What OpenQuestion holds
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.