ArticleVirology2011
Activation of protein kinase R is required for induction of stress granules by respiratory syncytial virus but dispensable for viral replication.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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
52 citing papers in PubMed, 75 citations in OpenAlex.
- Respiratory syncytial virus (RSV) enhances translation of virus-resembling AU-rich host transcripts.Virology journal · 2025Article
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- Identification and characterization of host miRNAs that target the mouse mammary tumour virus (MMTV) genome.Open biology · 2024Article
- Activation of protein kinase receptor (PKR) plays a pro-viral role in mammarenavirus-infected cells.Journal of virology · 2024Article
- Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.PLoS biology · 2023Article
- The Interplay of Genital Herpes with Cellular Processes: A Pathogenesis and Therapeutic Perspective.Viruses · 2023Review
- Stress Granules as Causes and Consequences of Translation Suppression.Antioxidants & redox signaling · 2023Review
- Multiple functions of stress granules in viral infection at a glance.Frontiers in microbiology · 2023Review
- Stress granules: potential therapeutic targets for infectious and inflammatory diseases.Frontiers in immunology · 2023Review
- Exploration of nanozymes in viral diagnosis and therapy.Exploration (Beijing, China) · 2022Review
- Host Defence RNases as Antiviral Agents against Enveloped Single Stranded RNA Viruses.Virulence · 2021Review
- Review
- The Regulation of Integrated Stress Response Signaling Pathway on Viral Infection and Viral Antagonism.Frontiers in microbiology · 2021Review
- Review
- The Race between Host Antiviral Innate Immunity and the Immune Evasion Strategies of Herpes Simplex Virus 1.Microbiology and molecular biology reviews : MMBR · 2020Review
- Respiratory Syncytial Virus Sequesters NF-κB Subunit p65 to Cytoplasmic Inclusion Bodies To Inhibit Innate Immune Signaling.Journal of virology · 2020Article
- Innate Immune Evasion by Human Respiratory RNA Viruses.Journal of innate immunity · 2020Review
- Viral Regulation of RNA Granules in Infected Cells.Virologica Sinica · 2019Review
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
- Stress Granule Formation is One of the Early Antiviral Mechanisms for Host Cells Against Coxsackievirus B Infection.Virologica Sinica · 2018Article
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 1 institution in 1 country.
Funding
Abstract
We performed experiments to determine the effect of PKR activation on respiratory syncytial virus (RSV) replication. We first determined that RSV infection activates PKR which induces the phosphorylation of eIF2α, resulting in the formation of host stress granules. We used RNA interference to decrease endogenous PKR levels. RSV replication was not altered in cells deficient for PKR expression. However, RSV-mediated stress granule formation was significantly reduced in PKR-knockdown cells. As an alternative method to block PKR activation, we used treatment with the kinase inhibitor 2-aminopurine (2-AP). We observed that 2-AP treatment significantly reduced viral replication. We also treated PKR-knockdown cells with 2-AP and inoculated with RSV. Under these conditions, 2-AP treatment diminished viral replication in the absence of PKR expression. These results suggest that PKR activation has a minimal effect on RSV replication and that the antiviral effect of 2-AP during RSV infection likely occurs via a PKR-independent mechanism.
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.