ArticleJournal of virology2020
Retinoic Acid Inducible Gene I and Protein Kinase R, but Not Stress Granules, Mediate the Proinflammatory Response to Yellow Fever Virus.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Stress granules formed during infections with RNA viruses have significant virus-specific differences in generation and composition.PLoS biology · 2026Article
- The assembly of stress granules during foot-and-mouth disease virus infection is uncoupled from activation of cellular intrinsic antiviral signalling.PLoS pathogens · 2026Article
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- Yellow Fever Virus Interactomes Reveal Common and Divergent Strategies of Replication and Evolution for Mosquito-borne Flaviviruses.bioRxiv : the preprint server for biology · 2025Article
- TRBP modulates RLR signaling by inhibiting PKR-mediated antiviral stress granule formation.Scientific reports · 2025Article
- Pathogenesis and clinical management of arboviral diseases.World journal of virology · 2025Review
- Emerging roles of stress granules in liver diseases: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- Viral hijacking of hnRNPH1 unveils a G-quadruplex-driven mechanism of stress control.Cell host & microbe · 2024Article
- Cellular Stress: Modulator of Regulated Cell Death.Biology · 2023Review
- Stress Granules as Causes and Consequences of Translation Suppression.Antioxidants & redox signaling · 2023Review
- Nucleic acid-protein condensates in innate immune signaling.The EMBO journal · 2023Review
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Review
- The DEAD box RNA helicase DDX42 is an intrinsic inhibitor of positive-strand RNA viruses.EMBO reports · 2022Article
- The Railmap of Type I Interferon Induction: Subcellular Network Plan and How Viruses Can Change Tracks.Cells · 2022Review
- Review
- dsRNA-induced condensation of antiviral proteins modulates PKR activity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Roles of antiviral sensing and type I interferon signaling in the restriction of SARS-CoV-2 replication.iScience · 2022Article
- Flaviviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines.Frontiers in immunology · 2022Review
- A yellow fever virus NS4B inhibitor not only suppresses viral replication, but also enhances the virus activation of RIG-I-like receptor-mediated innate immune response.PLoS pathogens · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yellow fever virus (YFV) is an RNA virus primarily targeting the liver. Severe YF cases are responsible for hemorrhagic fever, plausibly precipitated by excessive proinflammatory cytokine response. Pathogen recognition receptors (PRRs), such as the cytoplasmic retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), and the viral RNA sensor protein kinase R (PKR), are known to initiate a proinflammatory response upon recognition of viral genomes. Here, we sought to reveal the main determinants responsible for the acute cytokine expression occurring in human hepatocytes following YFV infection. Using a RIG-I-defective human hepatoma cell line, we found that RIG-I largely contributes to cytokine secretion upon YFV infection. In infected RIG-I-proficient hepatoma cells, RIG-I was localized in stress granules. These granules are large aggregates of stalled translation preinitiation complexes known to concentrate RLRs and PKR and are so far recognized as hubs orchestrating RNA virus sensing. Stable knockdown of PKR in hepatoma cells revealed that PKR contributes to both stress granule formation and cytokine induction upon YFV infection. However, stress granule disruption did not affect the cytokine response to YFV infection, as assessed by small interfering RNA (siRNA)-knockdown-mediated inhibition of stress granule assembly. Finally, no viral RNA was detected in stress granules using a fluorescence
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.