ArticleJournal of virology2007
Activation of the beta interferon promoter by unnatural Sendai virus infection requires RIG-I and is inhibited by viral C proteins.
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 82 papers.
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Who cites it
82 citing papers in PubMed, 111 citations in OpenAlex.
- SARS-CoV-2 defective viral genomes from distinct genomic regions drive divergent interferon responses.PLoS pathogens · 2026Article
- A respiratory syncytial virus trailer sequence modulates viral replication and the generation and propagation kinetics of copy-back defective viral genomes.Journal of virology · 2026Article
- 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
- Immunostimulatory nucleic acid nanoparticles establish antiviral state to inhibit viral infection and replication.Journal of virology · 2026Article
- A Respiratory Syncytial Virus trailer sequence modulates viral replication and copy-back defective viral genome generation and propagation kinetics.bioRxiv : the preprint server for biology · 2025Article
- Validation of diverse and previously untraceable Sendai virus copyback viral genomes by direct RNA sequencing.Journal of virology · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Characterization of a recombinant Sendai virus vector encoding the small ruminant lentivirus gag-P25: antiviral properties in vitro and transgene expression in sheep.Veterinary research · 2025Article
- Identification, functional analysis, and clinical applications of defective viral genomes.Frontiers in microbiology · 2025Review
- Review
- Tailam paramyxovirus C protein inhibits viral replication.Journal of virology · 2024Article
- Influenza Defective Interfering Virus Promotes Multiciliated Cell Differentiation and Reduces the Inflammatory Response in Mice.Journal of virology · 2023Article
- Mitochondrial antiviral signaling protein: a potential therapeutic target in renal disease.Frontiers in immunology · 2023Review
- A Virus Is a Community: Diversity within Negative-Sense RNA Virus Populations.Microbiology and molecular biology reviews : MMBR · 2022Review
- High-Risk Mucosal Human Papillomavirus 16 (HPV16) E6 Protein and Cutaneous HPV5 and HPV8 E6 Proteins Employ Distinct Strategies To Interfere with Interferon Regulatory Factor 3-Mediated Beta Interferon Expression.Journal of virology · 2022Article
- Review
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- Overview of SARS-CoV-2 genome-encoded proteins.Science China. Life sciences · 2022Review
- C Proteins: Controllers of Orderly Paramyxovirus Replication and of the Innate Immune Response.Viruses · 2022Review
- Accumulation of copy-back viral genomes during respiratory syncytial virus infection is preceded by diversification of the copy-back viral genome population followed by selection.Virus evolution · 2022Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As infection with wild-type (wt) Sendai virus (SeV) normally activates beta interferon (IFN-beta) very poorly, two unnatural SeV infections were used to study virus-induced IFN-beta activation in mouse embryonic fibroblasts: (i) SeV-DI-H4, which is composed mostly of small, copyback defective interfering (DI) genomes and whose infection overproduces short 5'-triphosphorylated trailer RNAs (pppRNAs) and underproduces viral V and C proteins, and (ii) SeV-GFP(+/-), a coinfection that produces wt amounts of viral gene products but that also produces both green fluorescent protein (GFP) mRNA and its complement, which can form double-stranded RNA (dsRNA) with capped 5' ends. We found that (i) virus-induced signaling to IFN-beta depended predominantly on RIG-I (as opposed to mda-5) for both SeV infections, i.e., that RIG-I senses both pppRNAs and dsRNA without 5'-triphosphorylated ends, and (ii) it is the viral C protein (as opposed to V) that is primarily responsible for countering RIG-I-dependent signaling to IFN-beta. Nondefective SeV that cannot specifically express C proteins not only cannot prevent the effects of transfected poly(I-C) or (ppp)RNAs on IFN-beta activation but also synergistically enhances these effects. SeV-V(minus) infection, in contrast, behaves mostly like wt SeV and counteracts the effects of transfected poly(I-C) or (ppp)RNAs.
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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.