ArticlePLoS pathogens2015
Evidence for a Novel Mechanism of Influenza Virus-Induced Type I Interferon Expression by a Defective RNA-Encoded Protein.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Meta-analysis of genomic characteristics for antiviral influenza defective interfering particle prioritization.NAR genomics and bioinformatics · 2025Pooled it
- Pooled it
- Coevolutionary dynamics of viruses and their defective interfering particles.PLoS computational biology · 2026Article
- Coevolutionary dynamics of viruses and their defective interfering particles.bioRxiv : the preprint server for biology · 2025Article
- Matryoshka Dolls of Virus Evolution: The Internal Forces That Shape Viral Fate.Integrative and comparative biology · 2025Article
- Molecular Markers and Mechanisms of Influenza A Virus Cross-Species Transmission and New Host Adaptation.Viruses · 2024Review
- Cryptic proteins translated from deletion-containing viral genomes dramatically expand the influenza virus proteome.Nucleic acids research · 2024Article
- Cryptic proteins translated from deletion-containing viral genomes dramatically expand the influenza virus proteome.bioRxiv : the preprint server for biology · 2024Article
- Identification of the protein coding capability of coronavirus defective viral genomes by mass spectrometry.Virology journal · 2023Article
- Generation of "OP7 chimera" defective interfering influenza A particle preparations free of infectious virus that show antiviral efficacy in mice.Scientific reports · 2023Article
- Levels of Influenza A Virus Defective Viral Genomes Determine Pathogenesis in the BALB/c Mouse Model.Journal of virology · 2022Article
- Article
- Structure and Function of the Influenza Virus Transcription and Replication Machinery.Cold Spring Harbor perspectives in medicine · 2020Review
- Low-grade fever during COVID-19 convalescence: A report of 3 cases.World journal of clinical cases · 2020Article
- Article
- Article
- Regulation of MAVS Expression and Signaling Function in the Antiviral Innate Immune Response.Frontiers in immunology · 2020Review
- Safety, Immunogenicity, and Effectiveness of Defective Viral Particles Arising in Mast Cells Against Influenza in Mice.Frontiers in immunology · 2020Article
- Single-Cell Virus Sequencing of Influenza Infections That Trigger Innate Immunity.Journal of virology · 2019Article
- Cardiac glycosides decrease influenza virus replication by inhibiting cell protein translational machinery.American journal of physiology. Lung cellular and molecular physiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) defective RNAs are generated as byproducts of error-prone viral RNA replication. They are commonly derived from the larger segments of the viral genome and harbor deletions of various sizes resulting in the generation of replication incompatible viral particles. Furthermore, small subgenomic RNAs are known to be strong inducers of pattern recognition receptor RIG-I-dependent type I interferon (IFN) responses. The present study identifies a novel IAV-induced defective RNA derived from the PB2 segment of A/Thailand/1(KAN-1)/2004 (H5N1). It encodes a 10 kDa protein (PB2∆) sharing the N-terminal amino acid sequence of the parental PB2 protein followed by frame shift after internal deletion. PB2∆ induces the expression of IFNβ and IFN-stimulated genes by direct interaction with the cellular adapter protein MAVS, thereby reducing viral replication of IFN-sensitive viruses such as IAV or vesicular stomatitis virus. This induction of IFN is completely independent of the defective RNA itself that usually serves as pathogen-associated pattern and thus does not require the cytoplasmic sensor RIG-I. These data suggest that not only defective RNAs, but also some defective RNA-encoded proteins can act immunostimulatory. In this particular case, the KAN-1-induced defective RNA-encoded protein PB2∆ enhances the overwhelming immune response characteristic for highly pathogenic H5N1 viruses, leading to a more severe phenotype in vivo.
Indexed as
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.