ArticlePloS one2014
Syndecan 4 is involved in mediating HCV entry through interaction with lipoviral particle-associated apolipoprotein E.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- Single-cell and bulk RNA sequencing reveals specific Trem2 positive B cell subtype niche after myocardial infarction in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Hepatitis B virus entry, assembly, and egress.Microbiology and molecular biology reviews : MMBR · 2024Review
- The low-density lipoprotein receptor and apolipoprotein E associated with CCHFV particles mediate CCHFV entry into cells.Nature communications · 2024Article
- Biomarkers in Detection of Hepatitis C Virus Infection.Pathogens (Basel, Switzerland) · 2024Review
- Apolipoprotein E and viral infection: Risks and Mechanisms.Molecular therapy. Nucleic acids · 2023Review
- Article
- Impact of direct-acting antiviral regimens on hepatic and extrahepatic manifestations of hepatitis C virus infection.World journal of hepatology · 2022Review
- SPOCK1 Promotes the Development of Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Heparan Sulfate Proteoglycans in Viral Infection and Treatment: A Special Focus on SARS-CoV-2.International journal of molecular sciences · 2021Review
- Hepatitis C Virus Glycan-Dependent Interactions and the Potential for Novel Preventative Strategies.Pathogens (Basel, Switzerland) · 2021Review
- Molecular Crosstalk between the Hepatitis C Virus and the Extracellular Matrix in Liver Fibrogenesis and Early Carcinogenesis.Cancers · 2021Review
- Hepatitis C Virus Uses Host Lipids to Its Own Advantage.Metabolites · 2021Review
- The Importance of Glycans of Viral and Host Proteins in Enveloped Virus Infection.Frontiers in immunology · 2021Review
- Hepatitis C virus infection and tight junction proteins: The ties that bind.Biochimica et biophysica acta. Biomembranes · 2020Review
- Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process.International journal of molecular sciences · 2020Review
- 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
- Syndecan 4 Upregulation on Activated Langerhans Cells Counteracts Langerin Restriction to Facilitate Hepatitis C Virus Transmission.Frontiers in immunology · 2020Article
- Regulation of the Transferrin Receptor Recycling in Hepatitis C Virus-Replicating Cells.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is a major cause of liver disease worldwide and HCV infection represents a major health problem. HCV associates with host lipoproteins forming host/viral hybrid complexes termed lipoviral particles. Apolipoprotein E (apoE) is a lipoprotein component that interacts with heparan sulfate proteoglycans (HSPG) to mediate hepatic lipoprotein uptake, and may likewise mediate HCV entry. We sought to define the functional regions of apoE with an aim to identify critical apoE binding partners involved in HCV infection. Using adenoviral vectors and siRNA to modulate apoE expression we show a direct correlation of apoE expression and HCV infectivity, whereas no correlation exists with viral protein expression. Mutating the HSPG binding domain (HSPG-BD) of apoE revealed key residues that are critical for mediating HCV infection. Furthermore, a novel synthetic peptide that mimics apoE's HSPG-BD directly and competitively inhibits HCV infection. Genetic knockdown of the HSPG proteins syndecan (SDC) 1 and 4 revealed that SDC4 principally mediates HCV entry. Our data demonstrate that HCV uses apoE-SDC4 interactions to enter hepatoma cells and establish infection. Targeting apoE-SDC interactions could be an alternative strategy for blocking HCV entry, a critical step in maintaining chronic 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.