ArticlePLoS pathogens2016
Lipoprotein Receptors Redundantly Participate in Entry of Hepatitis C Virus.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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Who cites it
52 citing papers in PubMed, 89 citations in OpenAlex.
- Advances in molecular regulation and function of LDLR family in viral infection.Frontiers in microbiology · 2025Review
- Dual Receptor Targeting Ensures Uptake and Anticancer Efficacy of Low-Density Lipoprotein-Docosahexaenoic Acid Nanoparticles Across Breast Cancer Cell Subtypes.Breast cancer (Dove Medical Press) · 2025Article
- Porcine low-density lipoprotein receptor plays an important role in classical swine fever virus infection.Emerging microbes & infections · 2024Article
- Extracellular Vesicles as Drug Delivery System for Cancer Therapy.Pharmaceutics · 2024Review
- The low-density lipoprotein receptor and apolipoprotein E associated with CCHFV particles mediate CCHFV entry into cells.Nature communications · 2024Article
- LDLR is an entry receptor for Crimean-Congo hemorrhagic fever virus.Cell research · 2024Article
- Pseudorabies virus upregulates low-density lipoprotein receptors to facilitate viral entry.Journal of virology · 2024Article
- LDLR is used as a cell entry receptor by multiple alphaviruses.Nature communications · 2024Article
- The matrix metalloproteinase ADAM10 supports hepatitis C virus entry and cell-to-cell spread via its sheddase activity.PLoS pathogens · 2023Article
- GB Virus B and Hepatitis C Virus, Distantly Related Hepaciviruses, Share an Entry Factor, Claudin-1.Journal of virology · 2023Article
- Scavenger receptor class B type I genetic variants associated with disease severity in chronic hepatitis C virus infection.Journal of medical virology · 2023Article
- Exosomal targeting and its potential clinical application.Drug delivery and translational research · 2022Review
- Article
- Impact of direct-acting antiviral regimens on hepatic and extrahepatic manifestations of hepatitis C virus infection.World journal of hepatology · 2022Review
- Article
- SARS-CoV-2 infection as a trigger of humoral response against apolipoprotein A-1.European journal of clinical investigation · 2021Article
- Pervasive Positive Selection on Virus Receptors Driven by Host-Virus Conflicts in Mammals.Journal of virology · 2021Article
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Interdependent Impact of Lipoprotein Receptors and Lipid-Lowering Drugs on HCV Infectivity.Cells · 2021Article
- Lipid homeostasis and mevalonate pathway in COVID-19: Basic concepts and potential therapeutic targets.Progress in lipid research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scavenger receptor class B type 1 (SR-B1) and low-density lipoprotein receptor (LDLR) are known to be involved in entry of hepatitis C virus (HCV), but their precise roles and their interplay are not fully understood. In this study, deficiency of both SR-B1 and LDLR in Huh7 cells was shown to impair the entry of HCV more strongly than deficiency of either SR-B1 or LDLR alone. In addition, exogenous expression of not only SR-B1 and LDLR but also very low-density lipoprotein receptor (VLDLR) rescued HCV entry in the SR-B1 and LDLR double-knockout cells, suggesting that VLDLR has similar roles in HCV entry. VLDLR is a lipoprotein receptor, but the level of its hepatic expression was lower than those of SR-B1 and LDLR. Moreover, expression of mutant lipoprotein receptors incapable of binding to or uptake of lipid resulted in no or slight enhancement of HCV entry in the double-knockout cells, suggesting that binding and/or uptake activities of lipid by lipoprotein receptors are essential for HCV entry. In addition, rescue of infectivity in the double-knockout cells by the expression of the lipoprotein receptors was not observed following infection with pseudotype particles bearing HCV envelope proteins produced in non-hepatic cells, suggesting that lipoproteins associated with HCV particles participate in the entry through their interaction with lipoprotein receptors. Buoyant density gradient analysis revealed that HCV utilizes these lipoprotein receptors in a manner dependent on the lipoproteins associated with HCV particles. Collectively, these results suggest that lipoprotein receptors redundantly participate in the entry of HCV.
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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.