ArticleVirology2011
Failure to activate the IFN-β promoter by a paramyxovirus lacking an interferon antagonist.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 41 citations in OpenAlex.
- Detailed single-cell mapping of the transcriptional response to a virus infection driven by copy-back viral genomes.PLoS pathogens · 2026Article
- Detailed single-cell mapping of the transcriptional response to a virus infection driven by copy-back viral genomes.bioRxiv : the preprint server for biology · 2026Article
- Direct Antiviral Activity of IFN-Stimulated Genes Is Responsible for Resistance to Paramyxoviruses in ISG15-Deficient Cells.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Innate Intracellular Antiviral Responses Restrict the Amplification of Defective Virus Genomes of Parainfluenza Virus 5.Journal of virology · 2020Article
- Article
- Single-cell analysis of early antiviral gene expression reveals a determinant of stochastic IFNB1 expression.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- Reduced accumulation of defective viral genomes contributes to severe outcome in influenza virus infected patients.PLoS pathogens · 2017Article
- Review
- Loss of Sendai virus C protein leads to accumulation of RIG-I immunostimulatory defective interfering RNA.The Journal of general virology · 2017Article
- Single-cell studies of IFN-β promoter activation by wild-type and NS1-defective influenza A viruses.The Journal of general virology · 2017Article
- Article
- Bluetongue Virus NS4 Protein Is an Interferon Antagonist and a Determinant of Virus Virulence.Journal of virology · 2016Article
- Induction and Antagonism of Antiviral Responses in Respiratory Syncytial Virus-Infected Pediatric Airway Epithelium.Journal of virology · 2015Article
- Influenza virus activation of the interferon system.Virus research · 2015Review
- Porcine sapovirus replication is restricted by the type I interferon response in cell culture.The Journal of general virology · 2015Article
- An unbiased genetic screen reveals the polygenic nature of the influenza virus anti-interferon response.Journal of virology · 2014Article
- Activation of the interferon induction cascade by influenza a viruses requires viral RNA synthesis and nuclear export.Journal of virology · 2014Article
- The influence of viral RNA secondary structure on interactions with innate host cell defences.Nucleic acids research · 2014Article
- Generation of replication-proficient influenza virus NS1 point mutants with interferon-hyperinducer phenotype.PloS one · 2014Article
- Deep sequencing analysis of defective genomes of parainfluenza virus 5 and their role in interferon induction.Journal of virology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It is generally thought that pathogen-associated molecular patterns (PAMPs) responsible for triggering interferon (IFN) induction are produced during virus replication and, to limit the activation of the IFN response by these PAMPs, viruses encode antagonists of IFN induction. Here we have studied the induction of IFN by parainfluenza virus type 5 (PIV5) at the single-cell level, using a cell line expressing GFP under the control of the IFN-β promoter. We demonstrate that a recombinant PIV5 (termed PIV5-VΔC) that lacks a functional V protein (the viral IFN antagonist) does not activate the IFN-β promoter in the majority of infected cells. We conclude that viral PAMPs capable of activating the IFN induction cascade are not produced or exposed during the normal replication cycle of PIV5, and suggest instead that defective viruses are primarily responsible for inducing IFN during PIV5 infection in this system.
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Identifiers
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.