Evidence map›Paper›PMID 28363797›Full record

ArticleJournal of hepatology2017

Scavenger receptor class B member 1 (SCARB1) variants modulate hepatitis C virus replication cycle and viral load.

Sandra Westhaus, Maximilian Deest, Anna T X Nguyen, Frauke Stanke, Dirk Heckl, Rui Costa, Axel Schambach, Michael P Manns, Thomas Berg, Florian W R Vondran and 3 more

Abstract read
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In one paragraph

Article in Journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. The potential impacts of human genetics on virus emergence.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Sandra WesthausDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; Institute of Virology, University Hospital Essen, Essen, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany.
Maximilian DeestDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany; Institute for Molecular Biology, Hannover Medical School, Hannover, Germany.
Anna T X NguyenDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany; Institute for Molecular Biology, Hannover Medical School, Hannover, Germany.
Frauke StankeClinic for Pediatric Pneumology and Neonatology, Hannover Medical School, Hannover, Germany; German Center for Lung Research (DLZ), partner site BREATH.
Dirk HecklDepartment for Pediatric Hematology and Oncology, Hannover Medical School, Hannover, Germany.
Rui CostaDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany; Institute for Molecular Biology, Hannover Medical School, Hannover, Germany.
Axel SchambachDepartment Experimental Hematology, Hannover Medical School, Hannover, Germany.
Michael P MannsDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany.
Thomas BergDepartment of Gastroenterology and Rheumatology - Section Hepatology, University Hospital Leipzig, Leipzig, Germany.
Florian W R VondranGerman Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany; Department of General, Visceral and Transplant Surgery, Hannover Medical School, Hannover, Germany.
Christoph SarrazinMedical Clinic I, University Hospital Frankfurt, Frankfurt am Main, Germany; Medizinische Klinik II, St. Josefs-Hospital, Wiesbaden, Germany; German Center for Infection Research (DZIF); External Partner Site Frankfurt am Main, Germany.
Sandra CiesekDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; Institute of Virology, University Hospital Essen, Essen, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany.
Thomas von HahnDepartment of Gastroenterology, Hepatology und Endocrinology, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover-Braunschweig Site, Germany; Institute for Molecular Biology, Hannover Medical School, Hannover, Germany. Electronic address: vonHahn.Thomas@mh-hannover.de.
German Center for Infection Research · DEMedizinische Hochschule Hannover · DEGoethe University Frankfurt · DEUniversity Hospital Leipzig · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsThere are numerous coding and non-coding variants in the SCARB1 gene that encodes scavenger receptor class B member 1 (SR-BI), a key receptor for both high density lipoproteins and hepatitis C virus (HCV). Many have been linked to clinical phenotypes, yet their impact on the HCV replication cycle is incompletely understood. The aim of this study was to analyze the impact of these variants on the molecular biology and clinical course of HCV.

methodsWe analyzed key coding non-synonymous as well as non-coding SCARB1 variants using virological in vitro and human genetics approaches.

resultsNon-synonymous variants: S112F and T175A have greatly reduced HCV receptor function. When present on the cell surface, these variants are impaired in their ability to interact with HCV E2. Non-coding variants: The G allele in rs3782287 is associated with decreased viral load. Haplotype analysis confirmed these findings and identified haplotype rs3782287 A/rs5888 C as a risk allele associated with increased viral load. We also detected a trend towards lower hepatic SR-BI expression in individuals with the rs3782287 GG genotype associated with low viral load suggesting a potential underlying mechanism.

conclusionCoding and non-coding genetic SCARB1 variants modulate the HCV replication cycle and possibly clinical features of hepatitis C. These findings underscore the relevance of SR-BI as an HCV receptor and contribute to our understanding of inter-individual variation in HCV infection. LAY SUMMARY: The cell surface receptor SR-BI (scavenger receptor class B member 1), is essential for hepatitis C virus (HCV) entry into hepatocytes. Variations in the gene coding this receptor influence infectivity and viral load. We analyzed these variations to gain a better understanding of inter-individual differences over the course of HCV infection.

Indexed as

Cell LineGenetic VariationHepacivirusHepatitis CHost-Pathogen InteractionsHumansPolymorphism, Single NucleotideScavenger Receptors, Class BViral Envelope ProteinsViral LoadVirus InternalizationVirus Replicationglycoprotein E2, Hepatitis C virusSCARB1 protein, humanScavenger Receptors, Class BViral Envelope ProteinsHaplotypeHepatitis C virus (HCV)SCARB1 geneScavenger receptor class B type I (SR-BI)Single nucleotide polymorphism (SNP)

Identifiers

PMID28363797
OpenAlexW2598636063

What OpenQuestion holds

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Registered trials

None linked

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.