ArticleJournal of virology2012
Hepatitis C virus infection alters P-body composition but is independent of P-body granules.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Plant P-bodies in post-transcriptional control: Composition, dynamics, and context-dependent roles.Plant communications · 2026Review
- Review
- Review
- Effect of P-body component Mov10 on HCV virus production and infectivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- KSHV RNA-binding protein ORF57 inhibits P-body formation to promote viral multiplication by interaction with Ago2 and GW182.Nucleic acids research · 2019Article
- RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019Review
- Strategies for Success. Viral Infections and Membraneless Organelles.Frontiers in cellular and infection microbiology · 2019Review
- RNA decay is an antiviral defense in plants that is counteracted by viral RNA silencing suppressors.PLoS pathogens · 2018Article
- Review
- Review
- Hepatitis C Virus Exploitation of Processing Bodies.Journal of virology · 2016Review
- Review
- XRN1 stalling in the 5' UTR of Hepatitis C virus and Bovine Viral Diarrhea virus is associated with dysregulated host mRNA stability.PLoS pathogens · 2015Article
- Cytoplasmic RNA Granules and Viral Infection.Annual review of virology · 2014Article
- The P body protein LSm1 contributes to stimulation of hepatitis C virus translation, but not replication, by microRNA-122.Nucleic acids research · 2014Article
- Screening of small molecules affecting mammalian P-body assembly uncovers links with diverse intracellular processes and organelle physiology.RNA biology · 2013Article
- Manipulation of cellular processing bodies and their constituents by viruses.DNA and cell biology · 2013Article
- Review
- P-body components LSM1, GW182, DDX3, DDX6 and XRN1 are recruited to WNV replication sites and positively regulate viral replication.Virology · 2013Article
- Modulation of hepatitis C virus RNA abundance and virus release by dispersion of processing bodies and enrichment of stress granules.Virology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Processing bodies (P-bodies) are highly dynamic cytoplasmic granules conserved among eukaryotes. They are present under normal growth conditions and contain translationally repressed mRNAs together with proteins from the mRNA decay and microRNA (miRNA) machineries. We have previously shown that the core P-body components PatL1, LSm1, and DDX6 (Rck/p54) are required for hepatitis C virus (HCV) RNA replication; however, how HCV infection affects P-body granules and whether P-body granules per se influence the HCV life cycle remain unresolved issues. Here we show that HCV infection alters P-body composition by specifically changing the localization pattern of P-body components that are required for HCV replication. This effect was not related to an altered expression level of these components and could be reversed by inhibiting HCV replication with a polymerase inhibitor. Similar observations were obtained with a subgenomic replicon that supports only HCV translation and replication, indicating that these early steps of the HCV life cycle trigger the P-body alterations. Finally, P-body disruption by Rap55 depletion did not affect viral titers or HCV protein levels, demonstrating that the localization of PatL1, LSm1, and DDX6 in P-bodies is not required for their function on HCV. Thus, the HCV-induced changes on P-bodies are mechanistically linked to the function of specific P-body components in HCV RNA translation and replication; however, the formation of P-body granules is not required for HCV infection.
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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.