ArticleJournal of virology2007
Scavenger receptor BI and BII expression levels modulate hepatitis C virus infectivity.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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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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
76 citing papers in PubMed, 148 citations in OpenAlex.
- Receptors and Host Factors for Enterovirus Infection: Implications for Cancer Therapy.Cancers · 2024Review
- The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.Immunity, inflammation and disease · 2023Review
- Meta-analysis of the association between toll-like receptor gene polymorphisms and hepatitis C virus infection.Frontiers in microbiology · 2023Review
- Article
- Liver dysfunction during COVID-19 pandemic: Contributing role of associated factors in disease progression and severity.World journal of hepatology · 2022Review
- Liver damage in the context of SARS-CoV-2. Covid-19 treatment and its effects on the liver.Journal of medicine and life · 2022Review
- Cellular factors involved in the hepatitis C virus life cycle.World journal of gastroenterology · 2021Review
- Liver Impairment and Hematological Changes in Patients with Chronic Hepatitis C and COVID-19: A Retrospective Study after One Year of Pandemic.Medicina (Kaunas, Lithuania) · 2021Article
- COVID-19 and liver disease: mechanistic and clinical perspectives.Nature reviews. Gastroenterology & hepatology · 2021Review
- Hepatitis C Virus Entry: An Intriguingly Complex and Highly Regulated Process.International journal of molecular sciences · 2020Review
- Building a mechanistic mathematical model of hepatitis C virus entry.PLoS computational biology · 2019Article
- SCARF-1 promotes adhesion of CD4Scientific reports · 2017Article
- Roles of lipoprotein receptors in the entry of hepatitis C virus.World journal of hepatology · 2015Review
- Functional and Biochemical Characterization of Hepatitis C Virus (HCV) Particles Produced in a Humanized Liver Mouse Model.The Journal of biological chemistry · 2015Article
- AP-2-associated protein kinase 1 and cyclin G-associated kinase regulate hepatitis C virus entry and are potential drug targets.Journal of virology · 2015Article
- Impact of lipids and lipoproteins on hepatitis C virus infection and virus neutralization.World journal of gastroenterology · 2014Review
- Role of hypervariable region 1 for the interplay of hepatitis C virus with entry factors and lipoproteins.Journal of virology · 2014Article
- Unexpected structural features of the hepatitis C virus envelope protein 2 ectodomain.Journal of virology · 2014Review
- Scavenger receptor class B type I (SR-BI): a versatile receptor with multiple functions and actions.Metabolism: clinical and experimental · 2014Review
- Scavenger receptor class B type I and immune dysfunctions.Current opinion in endocrinology, diabetes, and obesity · 2014Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
Hepatitis C virus (HCV) enters cells via a pH- and clathrin-dependent endocytic pathway. Scavenger receptor BI (SR-BI) and CD81 are important entry factors for HCV internalization into target cells. The SR-BI gene gives rise to at least two mRNA splice variants, SR-BI and SR-BII, which differ in their C termini. SR-BI internalization remains poorly understood, but SR-BII is reported to endocytose via a clathrin-dependent pathway, making it an attractive target for HCV internalization. We demonstrate that HCV soluble E2 can interact with human SR-BI and SR-BII. Increased expression of SR-BI and SR-BII in the Huh-7.5 hepatoma cell line enhanced HCV strain J6/JFH and JFH infectivity, suggesting that endogenous levels of these receptors limit infection. Elevated expression of SR-BI, but not SR-BII, increased the rate of J6/JFH infection, which may reflect altered intracellular trafficking of the splice variants. In human plasma, HCV particles have been reported to be complexed with lipoproteins, suggesting an indirect interaction of the virus with SR-BI and other lipoprotein receptors. Plasma from J6/JFH-infected uPA-SCID mice transplanted with human hepatocytes demonstrates an increased infectivity for SR-BI/II-overexpressing Huh-7.5 cells. Plasma-derived J6/JFH infectivity was inhibited by an anti-E2 monoclonal antibody, suggesting that plasma virus interaction with SR-BI was glycoprotein dependent. Finally, anti-SR-BI antibodies inhibited the infectivity of cell culture- and plasma-derived J6/JFH, suggesting a critical role for SR-BI/II in 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.