ArticleVirologica Sinica2018
Stress Granule Formation is One of the Early Antiviral Mechanisms for Host Cells Against Coxsackievirus B Infection.
Article in Virologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Molecular basis of delayed BSMYV infection in diploid Musa balbisiana, a banana progenitor.Molecular biology reports · 2025Article
- Stress Granules in Infectious Disease: Cellular Principles and Dynamic Roles in Immunity and Organelles.International journal of molecular sciences · 2024Review
- Coxsackievirus B3-Induced mMicroorganisms · 2024Article
- Stress Granules Inhibit Coxsackievirus B3-Mediated Cell Death via Reduction of Mitochondrial Reactive Oxygen Species and Viral Extracellular Release.Journal of microbiology and biotechnology · 2023Article
- Review
- The PERK/PKR-eIF2α Pathway Negatively Regulates Porcine Hemagglutinating Encephalomyelitis Virus Replication by Attenuating Global Protein Translation and Facilitating Stress Granule Formation.Journal of virology · 2022Article
- The role of host eIF2α in viral infection.Virology journal · 2020Review
- Expression Profile and Function Analysis of Long Non-coding RNAs in the Infection of Coxsackievirus B3.Virologica Sinica · 2019Article
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress granules (SGs) are intracellular granules formed when cellular translation is blocked and have been reported to be involved in a variety of viral infections. Our previous studies revealed that SGs are involved in the coxsackievirus B (CVB) infection process, but the role of SGs in CVB infection has not been fully explored. In this study, we found that CVB type 3 (CVB3) could induce SG formation in the early phase of infection. Results showed that levels of CVB3 RNA and protein were significantly inhibited during the early stage of CVB3 infection by the elevated formation of SGs, while viral RNA and protein synthesis were significantly promoted when SG formation was blocked. Our findings suggest that SG formation is one of the early antiviral mechanisms for host cells against CVB infection.
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