scholarly journals Role of Scavenger Receptor Class B Type I in Hepatitis C Virus Entry: Kinetics and Molecular Determinants

2009 ◽  
Vol 84 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Maria Teresa Catanese ◽  
Helenia Ansuini ◽  
Rita Graziani ◽  
Thierry Huby ◽  
Martine Moreau ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Entry ◽  
Scavenger Receptor ◽  
Specific Protein ◽  
Early Event ◽  
Type I ◽  
Direct Role ◽  
Scavenger Receptor Class ◽  
Class B

ABSTRACT Scavenger receptor class B type I (SR-BI) is an essential receptor for hepatitis C virus (HCV) and a cell surface high-density-lipoprotein (HDL) receptor. The mechanism of SR-BI-mediated HCV entry, however, is not clearly understood, and the specific protein determinants required for the recognition of the virus envelope are not known. HCV infection is strictly linked to lipoprotein metabolism, and HCV virions may initially interact with SR-BI through associated lipoproteins before subsequent direct interactions of the viral glycoproteins with SR-BI occur. The kinetics of inhibition of cell culture-derived HCV (HCVcc) infection with an anti-SR-BI monoclonal antibody imply that the recognition of SR-BI by HCV is an early event of the infection process. Swapping and single-substitution mutants between mouse and human SR-BI sequences showed reduced binding to the recombinant soluble E2 (sE2) envelope glycoprotein, thus suggesting that the SR-BI interaction with the HCV envelope is likely to involve species-specific protein elements. Most importantly, SR-BI mutants defective for sE2 binding, although retaining wild-type activity for receptor oligomerization and binding to the physiological ligand HDL, were impaired in their ability to fully restore HCVcc infectivity when transduced into an SR-BI-knocked-down Huh-7.5 cell line. These findings suggest a specific and direct role for the identified residues in binding HCV and mediating virus entry. Moreover, the observation that different regions of SR-BI are involved in HCV and HDL binding supports the hypothesis that new therapeutic strategies aimed at interfering with virus/SR-BI recognition are feasible.

scholarly journals High Density Lipoproteins Facilitate Hepatitis C Virus Entry through the Scavenger Receptor Class B Type I

2005 ◽  
Vol 280 (9) ◽  
pp. 7793-7799 ◽  
Author(s):  
Cécile Voisset ◽  
Nathalie Callens ◽  
Emmanuelle Blanchard ◽  
Anne Op De Beeck ◽  
Jean Dubuisson ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Entry ◽  
Scavenger Receptor ◽  
High Density ◽  
High Density Lipoproteins ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B

Scavenger Receptor Class B Type I Mediates Cell Entry of Hepatitis C Virus

2008 ◽  
Vol 36 (6) ◽  
pp. 1319-1325 ◽  
Author(s):  
ZS Jia ◽  
DW Du ◽  
YF Lei ◽  
X Wei ◽  
W Yin ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cho Cells ◽  
Hepg2 Cells ◽  
Scavenger Receptor ◽  
Chinese Hamster ◽  
Hcv Infection ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B

This study assessed the functional role of human scavenger receptor class B type I (SR-BI) as a putative hepatitis C virus (HCV) receptor using Chinese hamster ovary (CHO) cells transfected with human SR-BI (CHO–huSR-BI). The expression of SR-BI by primary Tupaia hepatocytes (PTHs), human hepatocarcinoma cell line (HepG2) cells, untransfected CHO cells and CHO–huSR-BI cells was analysed by Western blotting. Receptor competition assays showed that anti-SR-BI antibodies that block the binding of soluble envelope glycoprotein E2 could prevent HCV infection. Pre-incubation of CHO–huSR-BI and HepG2 cells with anti-SR-BI antibodies resulted in marked inhibition of E2 binding. After incubation with HCV RNA-positive serum from a patient with chronic HCV infection, however, HCV infection could not be detected in CHO–huSR-BI cells, but was detected in PTHs. These results demonstrate that, whilst SR-BI represents an important cell surface molecule for HCV infection, the presence of SR-BI alone is insufficient for HCV entry.

scholarly journals The postbinding activity of scavenger receptor class B type I mediates initiation of hepatitis C virus infection and viral dissemination

Hepatology ◽  
2012 ◽  
Vol 57 (2) ◽  
pp. 492-504 ◽  
Author(s):  
Muhammad N. Zahid ◽  
Marine Turek ◽  
Fei Xiao ◽  
Viet Loan Dao Thi ◽  
Maryse Guérin ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Scavenger Receptor ◽  
Type I ◽  
Hepatitis C Virus Infection ◽  
Viral Dissemination ◽  
Scavenger Receptor Class ◽  
Class B

Scavenger Receptor Class B Type I is a Hepatitis C Virus Receptor on Human Dendritic Cells

2006 ◽  
Vol 44 (01) ◽  
Author(s):  
H Barth ◽  
EK Schnober ◽  
C Neumann-Haefelin ◽  
R Thimme ◽  
HE Blum ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Scavenger Receptor ◽  
Type I ◽  
Virus Receptor ◽  
Scavenger Receptor Class ◽  
Class B ◽  
Human Dendritic Cells

scholarly journals Scavenger receptor class B type I is a key host factor for hepatitis C virus infection required for an entry step closely linked to CD81

Hepatology ◽  
2007 ◽  
Vol 46 (6) ◽  
pp. 1722-1731 ◽  
Author(s):  
Mirjam B. Zeisel ◽  
George Koutsoudakis ◽  
Eva K. Schnober ◽  
Anita Haberstroh ◽  
Hubert E. Blum ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Scavenger Receptor ◽  
Host Factor ◽  
Type I ◽  
Hepatitis C Virus Infection ◽  
Scavenger Receptor Class ◽  
Class B

O.192 Scavenger receptor class B type I is a co-receptor for infection with cell culture-derived hepatitis C virus

2006 ◽  
Vol 36 ◽  
pp. S58
Author(s):  
M.B. Zeisel ◽  
E.K. Schnober ◽  
A. Haberstroh ◽  
D. Lavillette ◽  
F. Cosset ◽  
...  
Keyword(s):  
Cell Culture ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Scavenger Receptor ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B

scholarly journals Scavenger Receptor Class B Type I and Hepatitis C Virus Infection of Primary Tupaia Hepatocytes

2005 ◽  
Vol 79 (9) ◽  
pp. 5774-5785 ◽  
Author(s):  
Heidi Barth ◽  
Raffaele Cerino ◽  
Mirko Arcuri ◽  
Marco Hoffmann ◽  
Peter Schürmann ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Surface ◽  
Scavenger Receptor ◽  
Hcv Infection ◽  
Type I ◽  
Scavenger Receptor Class ◽  
Class B

ABSTRACT Hepatitis C virus (HCV) is a major cause of chronic hepatitis worldwide. The study of early steps during HCV infection has been hampered by the lack of suitable in vitro or in vivo models. Primary Tupaia hepatocytes (PTH) have been shown to be susceptible to HCV infection in vitro and in vivo. Human scavenger receptor class B type I (SR-BI) represents an HCV receptor candidate mediating the cellular binding of E2 glycoprotein to HepG2 hepatoma cells. However, the function of SR-BI for viral infection of hepatocytes is unknown. In this study, we used PTH to assess the functional role of SR-BI as a putative HCV receptor. Sequence analysis of cloned tupaia SR-BI revealed a high homology between tupaia and human SR-BI. Transfection of CHO cells with human or tupaia SR-BI but not mouse SR-BI cDNA resulted in cellular E2 binding, suggesting that E2-binding domains between human and tupaia SR-BI are highly conserved. Preincubation of PTH with anti-SR-BI antibodies resulted in marked inhibition of E2 or HCV-like particle binding. However, anti-SR-BI antibodies were not able to block HCV infection of PTH. In conclusion, our results demonstrate that SR-BI represents an important cell surface molecule for the binding of the HCV envelope to hepatocytes and suggest that other or additional cell surface molecules are required for the initiation of HCV infection. Furthermore, the structural and functional similarities between human and tupaia SR-BI indicate that PTH represent a useful model system to characterize the molecular interaction of the HCV envelope and SR-BI on primary hepatocytes.

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