ArticleThe Journal of biological chemistry2009
Low pH-dependent hepatitis C virus membrane fusion depends on E2 integrity, target lipid composition, and density of virus particles.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 87 citations in OpenAlex.
- Tetraspanins 10 and 15 support Venezuelan equine encephalitis virus replication in astrocytoma cells.Molecular biology of the cell · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- The matrix metalloproteinase ADAM10 supports hepatitis C virus entry and cell-to-cell spread via its sheddase activity.PLoS pathogens · 2023Article
- The Human Liver-Expressed Lectin CD302 Restricts Hepatitis C Virus Infection.Journal of virology · 2022Article
- Modeling the Structure-Activity Relationship of Arbidol Derivatives and Other SARS-CoV-2 Fusion Inhibitors Targeting the S2 Segment of the Spike Protein.Journal of chemical information and modeling · 2021Article
- Functions of Sphingolipids in Pathogenesis During Host-Pathogen Interactions.Frontiers in microbiology · 2021Review
- Host receptors: the key to establishing cells with broad viral tropism for vaccine production.Critical reviews in microbiology · 2020Review
- Hepatitis C Virus Entry: Protein Interactions and Fusion Determinants Governing Productive Hepatocyte Invasion.Cold Spring Harbor perspectives in medicine · 2020Review
- Hepatitis C virus leaves an epigenetic signature post cure of infection by direct-acting antivirals.PLoS genetics · 2019Article
- The Antiviral Drug Arbidol Inhibits Zika Virus.Scientific reports · 2018Article
- Hepatitis C Virus Strain-Dependent Usage of Apolipoprotein E Modulates Assembly Efficiency and Specific Infectivity of Secreted Virions.Journal of virology · 2017Article
- Regulated Entry of Hepatitis C Virus into Hepatocytes.Viruses · 2017Review
- Functional Analysis of Hepatitis C Virus (HCV) Envelope Protein E1 Using aJournal of virology · 2017Article
- [Research advances in the role of sphingolipids in HCV and HBV life cycles].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016Review
- Entry inhibitors: New advances in HCV treatment.Emerging microbes & infections · 2016Review
- The Synthetic Antiviral Drug Arbidol Inhibits Globally Prevalent Pathogenic Viruses.Journal of virology · 2016Article
- Impact of lipids and lipoproteins on hepatitis C virus infection and virus neutralization.World journal of gastroenterology · 2014Review
- Arbidol as a broad-spectrum antiviral: an update.Antiviral research · 2014Review
- Integrative functional genomics of hepatitis C virus infection identifies host dependencies in complete viral replication cycle.PLoS pathogens · 2014Article
- How hepatitis C virus invades hepatocytes: the mystery of viral entry.World journal of gastroenterology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is an enveloped, positive strand RNA virus of about 9.6 kb. Like all enveloped viruses, the HCV membrane fuses with the host cell membrane during the entry process and thereby releases the genome into the cytoplasm, initiating the viral replication cycle. To investigate the features of HCV membrane fusion, we developed an in vitro fusion assay using cell culture-produced HCV and fluorescently labeled liposomes. With this model we could show that HCV-mediated fusion can be triggered in a receptor-independent but pH-dependent manner and that fusion of the HCV particles with liposomes is dependent on the viral dose and on the lipid composition of the target membranes. In addition CBH-5, an HCV E2-specific antibody, inhibited fusion in a dose-dependent manner. Interestingly, point mutations in E2, known to abrogate HCV glycoprotein-mediated fusion in a cell-based assay, altered or even abolished fusion in the liposome-based assay. When assaying the fusion properties of HCV particles with different buoyant density, we noted higher fusogenicity of particles with lower density. This could be attributable to inherently different properties of low density particles, to association of these particles with factors stimulating fusion, or to co-flotation of factors enhancing fusion activity in trans. Taken together, these data show the important role of lipids of both the viral and target membranes in HCV-mediated fusion, point to a crucial role played by the E2 glycoprotein in the process of HCV fusion, and reveal an important behavior of HCV of different densities with regard to fusion.
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