ArticleFrontiers in immunology2020
Seneca Valley Virus 3C Protease Inhibits Stress Granule Formation by Disrupting eIF4GI-G3BP1 Interaction.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- The assembly of stress granules during foot-and-mouth disease virus infection is uncoupled from activation of cellular intrinsic antiviral signalling.PLoS pathogens · 2026Article
- Stiffness-related stress granules promote the metastasis of early-stage oral squamous cell carcinoma via anoikis resistance.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Senecavirus a can replicate in apical-out porcine intestinal organoids and induce stress granules and innate immune response.Virulence · 2025Article
- Virulence determinant of Senecavirus A: 3C protein functions as a protease to cleave viral polyprotein and host factors.Virulence · 2025Review
- Activation of eIF2α-ATF4 by endoplasmic reticulum-mitochondria coupling stress enhances COX2 expression and MSC-based therapeutic efficacy for rheumatoid arthritis.Stem cell research & therapy · 2025Article
- Role(s) of G3BPs in Human Pathogenesis.The Journal of pharmacology and experimental therapeutics · 2023Review
- Allosteric regulation of Senecavirus A 3Cpro proteolytic activity by an endogenous phospholipid.PLoS pathogens · 2023Article
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Seneca Valley virus 3CFrontiers in microbiology · 2023Review
- Review
- Article
- Seneca Valley Virus Induces DHX30 Cleavage to Antagonize Its Antiviral Effects.Journal of virology · 2022Article
- 2AB protein of Senecavirus A antagonizes selective autophagy and type I interferon production by degrading LC3 and MARCHF8.Autophagy · 2022Article
- Seneca Valley Virus 3CMicrobiology spectrum · 2022Article
- The game between host antiviral innate immunity and immune evasion strategies of senecavirus A - A cell biological perspective.Frontiers in immunology · 2022Review
- Seneca Valley Virus 3CFrontiers in microbiology · 2022Article
- Seneca Valley virus 3CVirulence · 2021Article
- Selective autophagy receptor SQSTM1/ p62 inhibits Seneca Valley virus replication by targeting viral VP1 and VP3.Autophagy · 2021Article
- Research Progress on the Structure and Function of G3BP.Frontiers in immunology · 2021Review
- Two Birds With One Stone: RNA Virus Strategies to Manipulate G3BP1 and Other Stress Granule Components.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress granules (SGs) are the sites of mRNA storage and related to the regulation of mRNA translation, which are dynamic structures in response to various environmental stresses and viral infections. Seneca Valley virus (SVV), an oncolytic RNA virus belonging to Picornaviridae family, can cause vesicular disease (VD) indistinguished from foot-and-mouth disease (FMD) and other pig VDs. In this study, we found that SVV induced SG formation in the early stage of infection in a PKR-eIF2α dependent manner, as demonstrated by the recruitment of marker proteins of G3BP1 and eIF4GI. Surprisingly, we found that downregulating SG marker proteins TIA1 or G3BP1, or expressing an eIF2α non-phosphorylatable mutant inhibited SG formation, but this inhibition of transient SG formation had no significant effect on SVV propagation. Depletion of G3BP1 significantly attenuated the activation of NF-κB signaling pathway. In addition, we found that SVV inhibited SG formation at the late stage of infection and 3C protease was essential for the inhibition depending on its enzyme activity. Furthermore, we also found that 3C protease blocked the SG formation by disrupting eIF4GI-G3BP1 interaction. Overall, our results demonstrate that SVV induces transient SG formation in an eIF2α phosphorylation and PKR-dependent manner, and that 3C protease inhibits SG formation by interfering eIF4GI-G3BP1 interaction.
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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.