ArticleJournal of virology2013
Encephalomyocarditis virus disrupts stress granules, the critical platform for triggering antiviral innate immune responses.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 143 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
- The assembly of stress granules during foot-and-mouth disease virus infection is uncoupled from activation of cellular intrinsic antiviral signalling.PLoS pathogens · 2026Article
- The multifaceted role of the viral 2A protease in enterovirus replication and antagonism of host antiviral responses.PLoS pathogens · 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
- TRBP modulates RLR signaling by inhibiting PKR-mediated antiviral stress granule formation.Scientific reports · 2025Article
- Convergent evolution of the G3BP1-binding motif in betacoronavirus nucleocapsid proteins.Virus evolution · 2025Article
- Heart-specific NFAT5 knockout suppresses type I interferon signaling and aggravates coxsackievirus-induced myocarditis.Basic research in cardiology · 2024Article
- Coxsackievirus B3-Induced mMicroorganisms · 2024Article
- Liquid-liquid phase separation in innate immunity.Trends in immunology · 2024Review
- Interaction between host G3BP and viral nucleocapsid protein regulates SARS-CoV-2 replication and pathogenicity.Cell reports · 2024Article
- Cellular Stress Responses against Coronavirus Infection: A Means of the Innate Antiviral Defense.Journal of microbiology and biotechnology · 2024Review
- Biomolecular phase separation in stress granule assembly and virus infection.Acta biochimica et biophysica Sinica · 2023Article
- African swine fever virus pS273R antagonizes stress granule formation by cleaving the nucleating protein G3BP1 to facilitate viral replication.The Journal of biological chemistry · 2023Article
- Article
- Development of FRET and Stress Granule Dual-Based System to Screen for Viral 3C Protease Inhibitors.Molecules (Basel, Switzerland) · 2023Article
- Review
- 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
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to stress, cells induce ribonucleoprotein aggregates, termed stress granules (SGs). SGs are transient loci containing translation-stalled mRNA, which is eventually degraded or recycled for translation. Infection of some viruses, including influenza A virus with a deletion of nonstructural protein 1 (IAVΔNS1), induces SG-like protein aggregates. Previously, we showed that IAVΔNS1-induced SGs are required for efficient induction of type I interferon (IFN). Here, we investigated SG formation by different viruses using green fluorescent protein (GFP)-tagged Ras-Gap SH3 domain binding protein 1 (GFP-G3BP1) as an SG probe. HeLa cells stably expressing GFP-G3BP1 were infected with different viruses, and GFP fluorescence was monitored live with time-lapse microscopy. SG formations by different viruses was classified into 4 different patterns: no SG formation, stable SG formation, transient SG formation, and alternate SG formation. We focused on encephalomyocarditis virus (EMCV) infection, which exhibited transient SG formation. We found that EMCV disrupts SGs by cleavage of G3BP1 at late stages of infection (>8 h) through a mechanism similar to that used by poliovirus. Expression of a G3BP1 mutant that is resistant to the cleavage conferred persistent formation of SGs as well as an enhanced induction of IFN and other cytokines at late stages of infection. Additionally, knockdown of endogenous G3BP1 blocked SG formation with an attenuated induction of IFN and potentiated viral replication. Taken together, our findings suggest a critical role of SGs as an antiviral platform and shed light on one of the mechanisms by which a virus interferes with host stress and subsequent antiviral responses.
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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.