ArticlePLoS pathogens2020
Norovirus infection results in eIF2α independent host translation shut-off and remodels the G3BP1 interactome evading stress granule formation.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Drivers of the paradigm shift in norovirus diagnostics: technological innovation, contextual demands, and collaborative synergy.Virology journal · 2026Review
- Proof of concept: targeted protein degradation of the stress granules component G3BP1 as an antiviral strategy against norovirus infection.Antimicrobial agents and chemotherapy · 2026Article
- GCN2 enhances host survival and drives eIF2α phosphorylation during mouse adenovirus type 1 infection.Journal of virology · 2025Article
- 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
- Single-cell transcriptional analysis of murine norovirus infection in a human intestinal cell line.Journal of virology · 2024Article
- Norovirus-mediated translation repression promotes macrophage cell death.PLoS pathogens · 2024Article
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- Article
- Review
- Targeting Nup358/RanBP2 by a viral protein disrupts stress granule formation.PLoS pathogens · 2022Article
- Temporal control of the integrated stress response by a stochastic molecular switch.Science advances · 2022Article
- Novel stress granule-like structures are induced via a paracrine mechanism during viral infection.Journal of cell science · 2022Article
- Horizontal gene transfer as a mechanism for the promiscuous acquisition of distinct classes of IRES by avian caliciviruses.Nucleic acids research · 2022Article
- Monitoring Virus-Induced Stress Granule Dynamics Using Long-Term Live-Cell Imaging.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Large scale discovery of coronavirus-host factor protein interaction motifs reveals SARS-CoV-2 specific mechanisms and vulnerabilities.Nature communications · 2021Article
- 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
- Genes with 5' terminal oligopyrimidine tracts preferentially escape global suppression of translation by the SARS-CoV-2 Nsp1 protein.RNA (New York, N.Y.) · 2021Article
- Membraneless organelles restructured and built by pandemic viruses: HIV-1 and SARS-CoV-2.Journal of molecular cell biology · 2021Review
- Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Viral infections impose major stress on the host cell. In response, stress pathways can rapidly deploy defence mechanisms by shutting off the protein synthesis machinery and triggering the accumulation of mRNAs into stress granules to limit the use of energy and nutrients. Because this threatens viral gene expression, viruses need to evade these pathways to propagate. Human norovirus is responsible for gastroenteritis outbreaks worldwide. Here we examined how norovirus interacts with the eIF2α signaling axis controlling translation and stress granules. While norovirus infection represses host cell translation, our mechanistic analyses revealed that eIF2α signaling mediated by the stress kinase GCN2 is uncoupled from translational stalling. Moreover, infection results in a redistribution of the RNA-binding protein G3BP1 to replication complexes and remodelling of its interacting partners, allowing the avoidance from canonical stress granules. These results define novel strategies by which norovirus undergo efficient replication whilst avoiding the host stress response and manipulating the G3BP1 interactome.
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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.