ArticleJournal of virology2018
Inhibition of Stress Granule Formation by Middle East Respiratory Syndrome Coronavirus 4a Accessory Protein Facilitates Viral Translation, Leading to Efficient Virus Replication.
Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Brazilian Society of Cardiology Guideline on Myocarditis - 2022.Arquivos brasileiros de cardiologia · 2022Guideline
- TRIM21 blocks DDX3X-driven stress granule formation during Mycobacterium tuberculosis infection via a non-canonical E3 ligase mechanism.PLoS pathogens · 2026Article
- Antagonism of stress granules key for SARS-CoV-2 infection and pathogenesis.bioRxiv : the preprint server for biology · 2026Article
- Evolution of a truncated nucleocapsid protein enhances SARS-CoV-2 fitness by suppressing antiviral responses.PLoS biology · 2026Article
- Key residues in SARS-CoV-2 NSP3 hypervariable region are necessary to modulate early stress granule activity.Journal of virology · 2026Article
- MERS-CoV accessory ORF proteins in innate immune evasion: an evidence-graded functional framework.Frontiers in immunology · 2026Review
- Key residues in SARS-CoV-2 NSP3 hyper variable region are necessary to modulate early stress granule activity.bioRxiv : the preprint server for biology · 2025Article
- Convergent evolution of the G3BP1-binding motif in betacoronavirus nucleocapsid proteins.Virus evolution · 2025Article
- Stress Granules in Infectious Disease: Cellular Principles and Dynamic Roles in Immunity and Organelles.International journal of molecular sciences · 2024Review
- Coronavirus S protein alters dsRNA accumulation and stress granule formation through regulation of ADAR1-p150 expression.Nucleic acids research · 2024Article
- SARS-CoV-2 Nucleocapsid Protein Antagonizes GADD34-Mediated Innate Immune Pathway through Atypical Foci.Molecules (Basel, Switzerland) · 2024Article
- Pifithrin-µ Induces Stress Granule Formation, Regulates Cell Survival, and Rewires Cellular Signaling.Cells · 2024Article
- The NSP3 protein of SARS-CoV-2 binds fragile X mental retardation proteins to disrupt UBAP2L interactions.EMBO reports · 2024Article
- In silico analysis of balsaminol as anti-viral agents targeting SARS-CoV-2 main protease, spike receptor binding domain and papain-like protease receptors.In silico pharmacology · 2024Article
- Unlocking the puzzle: non-defining mutations in SARS-CoV-2 proteome may affect vaccine effectiveness.Frontiers in public health · 2024Article
- SARS-CoV-2 hijacks fragile X mental retardation proteins for efficient infection.bioRxiv : the preprint server for biology · 2023Article
- Targeting SARS-CoV-2 Non-Structural Proteins.International journal of molecular sciences · 2023Review
- SARS-CoV-2 nucleocapsid protein inhibits the PKR-mediated integrated stress response through RNA-binding domain N2b.PLoS pathogens · 2023Article
- Biomolecular phase separation in stress granule assembly and virus infection.Acta biochimica et biophysica Sinica · 2023Article
- The Nucleocapsid Proteins of SARS-CoV-2 and Its Close Relative Bat Coronavirus RaTG13 Are Capable of Inhibiting PKR- and RNase L-Mediated Antiviral Pathways.Microbiology spectrum · 2023Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Stress granule (SG) formation is generally triggered as a result of stress-induced translation arrest. The impact of SG formation on virus replication varies among different viruses, and the significance of SGs in coronavirus (CoV) replication is largely unknown. The present study examined the biological role of SGs in Middle East respiratory syndrome (MERS)-CoV replication. The MERS-CoV 4a accessory protein is known to inhibit SG formation in cells in which it was expressed by binding to double-stranded RNAs and inhibiting protein kinase R (PKR)-mediated phosphorylation of the α subunit of eukaryotic initiation factor 2 (eIF2α). Replication of MERS-CoV lacking the genes for 4a and 4b (MERS-CoV-Δp4), but not MERS-CoV, induced SG accumulation in MERS-CoV-susceptible HeLa/CD26 cells, while replication of both viruses failed to induce SGs in Vero cells, demonstrating cell type-specific differences in MERS-CoV-Δp4-induced SG formation. MERS-CoV-Δp4 replicated less efficiently than MERS-CoV in HeLa/CD26 cells, and inhibition of SG formation by small interfering RNA-mediated depletion of the SG components promoted MERS-CoV-Δp4 replication, demonstrating that SG formation was detrimental for MERS-CoV replication. Inefficient MERS-CoV-Δp4 replication was not due to either the induction of type I and type III interferons or the accumulation of viral mRNAs in the SGs. Rather, it was due to the inefficient translation of viral proteins, which was caused by high levels of PKR-mediated eIF2α phosphorylation and likely by the confinement of various factors that are required for translation in the SGs. Finally, we established that deletion of the 4a gene alone was sufficient for inducing SGs in infected cells. Our study revealed that 4a-mediated inhibition of SG formation facilitates viral translation, leading to efficient MERS-CoV 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.