ArticleJournal of virology2014
Measles virus C protein impairs production of defective copyback double-stranded viral RNA and activation of protein kinase R.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
73 citing papers in PubMed, 99 citations in OpenAlex.
- Minor differences in the untranslated regions of measles vector additional transcription units are reflected by differential immunogenicity of encoded MERS-CoV Spike antigen.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
- Variable and conserved features of copy-back viral genome populations generatedJournal of virology · 2026Article
- TSniffer: unbiased de novo identification of RNA editing sites and quantification of editing activity in RNA-seq data.Genome biology · 2026Article
- Discontinuous EBOV RNA synthesis events in patients with Ebola virus disease and their relationship to viral load and outcome of infection.Journal of virology · 2025Article
- AnViruses · 2025Article
- Mitochondrial targeting by measles virus nucleoprotein modulates viral spread in human airway epithelium.PLoS pathogens · 2025Article
- Designing a cellular MicroRNA-based approach to silence bat-borne Nipah virus genes.Journal of neurovirology · 2025Article
- Structure of the measles virus ternary polymerase complex.Nature communications · 2025Article
- The measles virus matrix F50S mutation from a lethal case of subacute sclerosing panencephalitis promotes receptor-independent neuronal spread.Journal of virology · 2025Article
- Evaluating the potential of anti-dsRNA antibodies as an alternative viral sensing tool in encephalitides of different species.Frontiers in veterinary science · 2025Article
- Host WD repeat-containing protein 5 inhibits protein kinase R-mediated integrated stress response during measles virus infection.Journal of virology · 2024Article
- Review
- Tailam paramyxovirus C protein inhibits viral replication.Journal of virology · 2024Article
- 3D Cryo-Correlative Methods to Study Virus Structure and Dynamics Within Cells.Sub-cellular biochemistry · 2024Review
- Molecular Analysis of Copy-Back Defective Interfering RNAs of Morbilliviruses.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.PLoS biology · 2023Article
- Interferon-independent processes constrain measles virus cell-to-cell spread in primary human airway epithelial cells.Microbiology spectrum · 2023Article
- Host-mediated RNA editing in viruses.Biology direct · 2023Review
- Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Measles virus (MV) lacking expression of C protein (C(KO)) is a potent activator of the double-stranded RNA (dsRNA)-dependent protein kinase (PKR), whereas the isogenic parental virus expressing C protein is not. Here, we demonstrate that significant amounts of dsRNA accumulate during C(KO) mutant infection but not following parental virus infection. dsRNA accumulated during late stages of infection and localized with virus replication sites containing N and P proteins. PKR autophosphorylation and stress granule formation correlated with the timing of dsRNA appearance. Phospho-PKR localized to dsRNA-containing structures as revealed by immunofluorescence. Production of dsRNA was sensitive to cycloheximide but resistant to actinomycin D, suggesting that dsRNA is a viral product. Quantitative PCR (qPCR) analyses revealed reduced viral RNA synthesis and a steepened transcription gradient in C(KO) virus-infected cells compared to those in parental virus-infected cells. The observed alterations were further reflected in lower viral protein expression levels and reduced C(KO) virus infectious yield. RNA deep sequencing confirmed the viral RNA expression profile differences seen by qPCR between C(KO) mutant and parental viruses. After one subsequent passage of the C(KO) virus, defective interfering RNA (DI-RNA) with a duplex structure was obtained that was not seen with the parental virus. We conclude that in the absence of C protein, the amount of PKR activator RNA, including DI-RNA, is increased, thereby triggering innate immune responses leading to impaired MV growth.
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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.