ArticleJournal of virology2011
Poliovirus-mediated disruption of cytoplasmic processing bodies.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 111 citations in OpenAlex.
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- The Rice Stripe Virus p2 Interacts With Lsm1 and Disrupts the Lsm1-Lsm4 Complex to Facilitate the Viral infection.Molecular plant pathology · 2026Article
- Equine infectious anemia virus blocks interferon responses through Rev-mediated activation of the stress granule-PKR-eIF2α pathway.PLoS pathogens · 2026Article
- The anti-viral protein Shiftless blocks p-body formation during KSHV infection.The Journal of general virology · 2026Article
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- The Seneca Valley virus 3C protease cleaves DCP1A to attenuate its antiviral effects.Veterinary research · 2025Article
- Suppression of double-stranded RNA sensing in cancer: molecular mechanisms and therapeutic potential.Biochemical Society transactions · 2024Review
- Modulation of nucleotide metabolism by picornaviruses.PLoS pathogens · 2024Article
- The main protease of SARS-CoV-2 cleaves histone deacetylases and DCP1A, attenuating the immune defense of the interferon-stimulated genes.The Journal of biological chemistry · 2023Article
- Review
- Kaposi's sarcoma-associated herpesvirus (KSHV) utilizes the NDP52/CALCOCO2 selective autophagy receptor to disassemble processing bodies.PLoS pathogens · 2023Article
- Human coronaviruses disassemble processing bodies.PLoS pathogens · 2022Article
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- Minding the message: tactics controlling RNA decay, modification, and translation in virus-infected cells.Genes & development · 2022Review
- Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function.PLoS pathogens · 2022Article
- Enterovirus 71 2A Protease Inhibits P-Body Formation To Promote Viral RNA Synthesis.Journal of virology · 2021Article
- Innate immune evasion mediated by picornaviral 3C protease: Possible lessons for coronaviral 3C-like protease?Reviews in medical virology · 2021Review
- Review
- RNA-Binding Proteins at the Host-Pathogen Interface Targeting Viral Regulatory Elements.Viruses · 2021Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Metazoan cells form cytoplasmic mRNA granules such as stress granules (SG) and processing bodies (P bodies) that are proposed to be sites of aggregated, translationally silenced mRNAs and mRNA degradation. Poliovirus (PV) is a plus-strand RNA virus containing a genome that is a functional mRNA; thus, we investigated if PV antagonizes the processes that lead to formation of these structures. We have previously shown that PV infection inhibits the ability of cells to form stress granules by cleaving RasGAP-SH3-binding protein (G3BP). Here, we show that P bodies are also disrupted during PV infection in cells by 4 h postinfection. The disruption of P bodies is more rapid and more complete than disruption of stress granules. The kinetics of P body disruption correlated with production of viral proteinases and required substantial viral gene product expression. The organizing mechanism that forms P body foci in cells is unknown; however, potential scaffolding, aggregating, or other regulatory proteins found in P bodies were investigated for degradation. Two factors involved in 5'-end mRNA decapping and degradation, Xrn1 and Dcp1a, and the 3' deadenylase complex component Pan3 underwent accelerated degradation during infection, and Dcp1a may be a direct substrate of PV 3C proteinase. Several other key factors proposed to be essential for P body formation, GW182, Edc3, and Edc4, were unaffected by poliovirus infection. Since deadenylation has been reported to be required for P body formation, viral inhibition of deadenylation, through Pan3 degradation, is a potential mechanism of P body disruption.
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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.