ArticleJournal of hepatology2017
Continuous de novo generation of spatially segregated hepatitis C virus replication organelles revealed by pulse-chase imaging.
Article in Journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 21 citations in OpenAlex.
- Disrupted glycosylphosphatidylinositol anchoring induces ER stress and restricts enterovirus infection.PLoS pathogens · 2025Article
- The HCV-Dependent Inhibition of Nrf1/ARE-Mediated Gene Expression Favours Viral Morphogenesis.Viruses · 2025Article
- Review
- Construction of coxsackievirus B5 viruses with luciferase reporters and their applications in vitro and in vivo.Virologica Sinica · 2023Article
- Regulatory Role of Phospholipids in Hepatitis C Virus Replication and Protein Function.Pathogens (Basel, Switzerland) · 2022Review
- Life cycle process dependencies of positive-sense RNA viruses suggest strategies for inhibiting productive cellular infection.Journal of the Royal Society, Interface · 2021Article
- High-Order Epistasis and Functional Coupling of Infection Steps Drive Virus Evolution toward Independence from a Host Pathway.Microbiology spectrum · 2021Article
- Reverse Genetic Approaches for the Generation of Full Length and Subgenomic Replicon of EV71 Virus.Frontiers in microbiology · 2021Article
- Whole Lotta Lipids-from HCV RNA Replication to the Mature Viral Particle.International journal of molecular sciences · 2020Review
- Nir2 Is an Effector of VAPs Necessary for Efficient Hepatitis C Virus Replication and Phosphatidylinositol 4-Phosphate Enrichment at the Viral Replication Organelle.Journal of virology · 2019Article
- HCV Pit Stop at the Lipid Droplet: Refuel Lipids and Put on a Lipoprotein Coat before Exit.Cells · 2019Review
- HCV NS5A dimer interface residues regulate HCV replication by controlling its self-interaction, hyperphosphorylation, subcellular localization and interaction with cyclophilin A.PLoS pathogens · 2018Article
- Hepatitis C Virus Replication Depends on Endosomal Cholesterol Homeostasis.Journal of virology · 2018Article
- SNAP-tagged Chikungunya Virus Replicons Improve Visualisation of Non-Structural Protein 3 by Fluorescence Microscopy.Scientific reports · 2017Article
- NS5A inhibitors unmask differences in functional replicase complex half-life between different hepatitis C virus strains.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsLike all positive-sense RNA viruses, hepatitis C virus (HCV) induces host membrane alterations for its replication. In chronically infected cells, it is not known whether these viral replication organelles are being continually resupplied by newly synthesized viral proteins in situ, or whether they are generated de novo. Here we aimed to study temporal events in replication organelles formation and maturation.
methodsHere we use pulse-chase labeling in combination with confocal microscopy, correlative light electron microscopy and biochemical methods to identify temporally distinct populations of replication organelles in living cells and study the formation, morphogenesis as well as compositional and functional changes of replication organelles over time.
resultsWe found that HCV replication organelles are continuously generated de novo at spatially distinct sites from preformed ones. This process is accompanied by accumulated intracellular membrane alteration, increased cholesterol delivery, NS5A phosphorylation, and positive-strand RNA content, and by eventual association with HCV core protein around lipid droplets. Generation of spatially segregated foci requires viral NS5A and the host factors phosphatidylinositol 4-kinase and oxysterol-binding protein, while association of foci with lipid droplets requires cholesterol.
conclusionsOur results reveal that HCV replication organelles are not static structures, but instead are continuously generated and dynamically change in composition and possibly also in function. LAY SUMMARY: Hepatitis C virus replication membrane structures are continuously generated at spatially distinct sites. New replication organelles are different in composition, and possibly also in function, compared to old replication organelles.
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