ArticlePLoS pathogens2009
Receptor complementation and mutagenesis reveal SR-BI as an essential HCV entry factor and functionally imply its intra- and extra-cellular domains.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 124 citations in OpenAlex.
- Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia.Journal of lipid research · 2010Trial
- Interplay of host and viral genetic variations in modulating antibody responses to genotype 3a hepatitis C virus: Implications for vaccine design.Cell reports · 2025Article
- The low-density lipoprotein receptor and apolipoprotein E associated with CCHFV particles mediate CCHFV entry into cells.Nature communications · 2024Article
- The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.Immunity, inflammation and disease · 2023Review
- Neurological aspects of SARS-CoV-2 infection: lipoproteins and exosomes as Trojan horses.Trends in endocrinology and metabolism: TEM · 2022Review
- Prognostic significance of temporal changes of lipid profile in COVID-19 patients.Obesity medicine · 2021Article
- Hepatitis C Virus Uses Host Lipids to Its Own Advantage.Metabolites · 2021Review
- Native High-Density Lipoproteins (HDL) with Higher Paraoxonase Exerts a Potent Antiviral Effect against SARS-CoV-2 (COVID-19), While Glycated HDL Lost the Antiviral Activity.Antioxidants (Basel, Switzerland) · 2021Article
- The roles of lipids in SARS-CoV-2 viral replication and the host immune response.Journal of lipid research · 2021Review
- Declined serum high density lipoprotein cholesterol is associated with the severity of COVID-19 infection.Clinica chimica acta; international journal of clinical chemistry · 2020Article
- Hepatitis C virus infection and tight junction proteins: The ties that bind.Biochimica et biophysica acta. Biomembranes · 2020Review
- An alternate conformation of HCV E2 neutralizing face as an additional vaccine target.Science advances · 2020Article
- Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process.International journal of molecular sciences · 2020Review
- Hepatitis C Virus Entry: Protein Interactions and Fusion Determinants Governing Productive Hepatocyte Invasion.Cold Spring Harbor perspectives in medicine · 2020Review
- Hepatitis C Virus Structure: Defined by What It Is Not.Cold Spring Harbor perspectives in medicine · 2020Review
- Immune Cell Trafficking to the Liver.Transplantation · 2019Review
- Scavenger receptor-C acts as a receptor for Bacillus thuringiensis vegetative insecticidal protein Vip3Aa and mediates the internalization of Vip3Aa via endocytosis.PLoS pathogens · 2018Article
- A protein coevolution method uncovers critical features of the Hepatitis C Virus fusion mechanism.PLoS pathogens · 2018Article
- Hepatitis C virus-apolipoprotein interactions: molecular mechanisms and clinical impact.Expert review of proteomics · 2017Review
- Role of Conserved E2 Residue W420 in Receptor Binding and Hepatitis C Virus Infection.Journal of virology · 2016Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HCV entry into cells is a multi-step and slow process. It is believed that the initial capture of HCV particles by glycosaminoglycans and/or lipoprotein receptors is followed by coordinated interactions with the scavenger receptor class B type I (SR-BI), a major receptor of high-density lipoprotein (HDL), the CD81 tetraspanin, and the tight junction protein Claudin-1, ultimately leading to uptake and cellular penetration of HCV via low-pH endosomes. Several reports have indicated that HDL promotes HCV entry through interaction with SR-BI. This pathway remains largely elusive, although it was shown that HDL neither associates with HCV particles nor modulates HCV binding to SR-BI. In contrast to CD81 and Claudin-1, the importance of SR-BI has only been addressed indirectly because of lack of cells in which functional complementation assays with mutant receptors could be performed. Here we identified for the first time two cell types that supported HCVpp and HCVcc entry upon ectopic SR-BI expression. Remarkably, the undetectable expression of SR-BI in rat hepatoma cells allowed unambiguous investigation of human SR-BI functions during HCV entry. By expressing different SR-BI mutants in either cell line, our results revealed features of SR-BI intracellular domains that influence HCV infectivity without affecting receptor binding and stimulation of HCV entry induced by HDL/SR-BI interaction. Conversely, we identified positions of SR-BI ectodomain that, by altering HCV binding, inhibit entry. Finally, we characterized alternative ectodomain determinants that, by reducing SR-BI cholesterol uptake and efflux functions, abolish HDL-mediated infection-enhancement. Altogether, we demonstrate that SR-BI is an essential HCV entry factor. Moreover, our results highlight specific SR-BI determinants required during HCV entry and physiological lipid transfer functions hijacked by HCV to favor 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.