ArticlemBio2019
Mouse Norovirus Infection Arrests Host Cell Translation Uncoupled from the Stress Granule-PKR-eIF2α Axis.
Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- Assembly of lipid droplet-associated ring structures in hepatitis C virus-infected cells via liquid-liquid phase separation (LLPS) and non-LLPS mechanisms.Journal of virology · 2026Article
- Proof of concept: targeted protein degradation of the stress granules component G3BP1 as an antiviral strategy against norovirus infection.Antimicrobial agents and chemotherapy · 2026Article
- The SHFV nsp2 and nucleocapsid proteins recruit G3BP1 to sites of viral replication, but stress granules are not induced by the infection.Journal of virology · 2025Article
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- Role of endoplasmic reticulum stress in cell apoptosis induced by duck hepatitis A virus type 1 infection.Frontiers in immunology · 2025Article
- Aggregation of Stress Granules Induced by Hypoxia and Lipopolysaccharide via PKR-p-eIF2α Pathway and 4EBP1 Pathway Inhibits the Inflammatory Response in Peri-Implantitis.Journal of inflammation research · 2025Article
- Norovirus-mediated translation repression promotes macrophage cell death.PLoS pathogens · 2024Article
- Myeloid PTEN loss affects the therapeutic response by promoting stress granule assembly and impairing phagocytosis by macrophages in breast cancer.Cell death discovery · 2024Article
- Infectious bursal disease virus VP5 triggers host shutoff in a transcription-dependent manner.mBio · 2024Article
- African swine fever virus RNA polymerase subunits C315R and H359L inhibition host translation by activating the PKR-eIF2a pathway and suppression inflammatory responses.Frontiers in microbiology · 2024Article
- Biomolecular phase separation in stress granule assembly and virus infection.Acta biochimica et biophysica Sinica · 2023Article
- Review
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Multiple functions of stress granules in viral infection at a glance.Frontiers in microbiology · 2023Review
- Horizontal gene transfer as a mechanism for the promiscuous acquisition of distinct classes of IRES by avian caliciviruses.Nucleic acids research · 2022Article
- Bacterial extracellular vesicles control murine norovirus infection through modulation of antiviral immune responses.Frontiers in immunology · 2022Article
- Interferon responses to norovirus infections: current and future perspectives.The Journal of general virology · 2021Review
- Murine Norovirus Infection Results in Anti-inflammatory Response Downstream of Amino Acid Depletion in Macrophages.Journal of virology · 2021Article
- SARS-CoV-2 suppresses IFNβ production mediated by NSP1, 5, 6, 15, ORF6 and ORF7b but does not suppress the effects of added interferon.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The integrated stress response (ISR) is a cellular response system activated upon different types of stresses, including viral infection, to restore cellular homeostasis. However, many viruses manipulate this response for their own advantage. In this study, we investigated the association between murine norovirus (MNV) infection and the ISR and demonstrate that MNV regulates the ISR by activating and recruiting key ISR host factors. We observed that during MNV infection, there is a progressive increase in phosphorylated eukaryotic initiation factor 2α (p-eIF2α), resulting in the suppression of host translation, and yet MNV translation still progresses under these conditions. Interestingly, the shutoff of host translation also impacts the translation of key signaling cytokines such as beta interferon, interleukin-6, and tumor necrosis factor alpha. Our subsequent analyses revealed that the phosphorylation of eIF2α was mediated via protein kinase R (PKR), but further investigation revealed that PKR activation, phosphorylation of eIF2α, and translational arrest were uncoupled during infection. We further observed that stress granules (SGs) are not induced during MNV infection and that MNV can restrict SG nucleation and formation. We observed that MNV recruited the key SG nucleating protein G3BP1 to its replication sites and intriguingly the silencing of G3BP1 negatively impacts MNV replication. Thus, it appears that MNV utilizes G3BP1 to enhance replication but equally to prevent SG formation, suggesting an anti-MNV property of SGs. Overall, this study highlights MNV manipulation of SGs, PKR, and translational control to regulate cytokine translation and to promote viral replication.
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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.