ArticleJournal of virology2013
Different requirements for scavenger receptor class B type I in hepatitis C virus cell-free versus cell-to-cell transmission.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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
54 citing papers in PubMed, 78 citations in OpenAlex.
- Safety and antiviral activity of the HCV entry inhibitor ITX5061 in treatment-naive HCV-infected adults: a randomized, double-blind, phase 1b study.The Journal of infectious diseases · 2014Trial
- Characterization of the virus-host RNA-RNA interactome across important human pathogenic RNA viruses.PLoS pathogens · 2026Article
- Beyond Viral Restriction: The Metabolic Dimensions of Interferon-Stimulated Genes in Antiviral Immunity.Viruses · 2026Review
- Review
- Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes.Journal of virology · 2024Article
- Article
- Scavenger receptor class B type I genetic variants associated with disease severity in chronic hepatitis C virus infection.Journal of medical virology · 2023Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- HCV Spread Kinetics Reveal Varying Contributions of Transmission Modes to Infection Dynamics.Viruses · 2021Article
- Virus-Mediated Cell-Cell Fusion.International journal of molecular sciences · 2020Review
- Hepatitis C virus infection and tight junction proteins: The ties that bind.Biochimica et biophysica acta. Biomembranes · 2020Review
- Host-Directed Antiviral Therapy.Clinical microbiology reviews · 2020Review
- Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process.International journal of molecular sciences · 2020Review
- Viral cell-to-cell spread: Conventional and non-conventional ways.Advances in virus research · 2020Review
- Clearance of hepatitis C virus is associated with early and potent but narrowly-directed, Envelope-specific antibodies.Scientific reports · 2019Article
- The interferon-inducible isoform of NCOA7 inhibits endosome-mediated viral entry.Nature microbiology · 2018Article
- HCV Reporter System (Viral Infection-Activated Split-Intein-Mediated Reporter System) for Testing Virus Cell-to-cell TransmissionBio-protocol · 2018Article
- Article
- Evolutionary Analysis Provides Insight Into the Origin and Adaptation of HCV.Frontiers in microbiology · 2018Article
- miRNA independent hepacivirus variants suggest a strong evolutionary pressure to maintain miR-122 dependence.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Hepatitis C virus (HCV) is believed to initially infect the liver through the basolateral side of hepatocytes, where it engages attachment factors and the coreceptors CD81 and scavenger receptor class B type I (SR-BI). Active transport toward the apical side brings the virus in close proximity of additional entry factors, the tight junction molecules claudin-1 and occludin. HCV is also thought to propagate via cell-to-cell spread, which allows highly efficient virion delivery to neighboring cells. In this study, we compared an adapted HCV genome, clone 2, characterized by superior cell-to cell spread, to its parental genome, J6/JFH-1, with the goal of elucidating the molecular mechanisms of HCV cell-to-cell transmission. We show that CD81 levels on the donor cells influence the efficiency of cell-to-cell spread and CD81 transfer between neighboring cells correlates with the capacity of target cells to become infected. Spread of J6/JFH-1 was blocked by anti-SR-BI antibody or in cells knocked down for SR-BI, suggesting a direct role for this receptor in HCV cell-to-cell transmission. In contrast, clone 2 displayed a significantly reduced dependence on SR-BI for lateral spread. Mutations in E1 and E2 responsible for the enhanced cell-to-cell spread phenotype of clone 2 rendered cell-free virus more susceptible to antibody-mediated neutralization. Our results indicate that although HCV can lose SR-BI dependence for cell-to-cell spread, vulnerability to neutralizing antibodies may limit this evolutionary option in vivo. Combination therapies targeting both the HCV glycoproteins and SR-BI may therefore hold promise for effective control of HCV dissemination.
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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.