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dc.contributor.authorZahid, Muhammad N
dc.contributor.authorTurek, Marine
dc.contributor.authorXiao, Fei
dc.contributor.authorThi, Viet Loan Dao
dc.contributor.authorGuérin, Maryse
dc.contributor.authorFofana, Isabel
dc.contributor.authorBachellier, Philippe
dc.contributor.authorThompson, John
dc.contributor.authorDelang, Leen
dc.contributor.authorNeyts, Johan
dc.contributor.authorBankwitz, Dorothea
dc.contributor.authorPietschmann, Thomas
dc.contributor.authorDreux, Marlène
dc.contributor.authorCosset, François-Loïc
dc.contributor.authorGrunert, Fritz
dc.contributor.authorBaumert, Thomas F
dc.contributor.authorZeisel, Mirjam B
dc.date.accessioned2013-06-24T09:46:00Z
dc.date.available2013-06-24T09:46:00Z
dc.date.issued2013-02
dc.identifier.citationThe postbinding activity of scavenger receptor class B type I mediates initiation of hepatitis C virus infection and viral dissemination. 2013, 57 (2):492-504 Hepatologyen_GB
dc.identifier.issn1527-3350
dc.identifier.pmid23081796
dc.identifier.doi10.1002/hep.26097
dc.identifier.urihttp://hdl.handle.net/10033/294439
dc.description.abstractScavenger receptor class B type I (SR-BI) is a high-density lipoprotein (HDL) receptor highly expressed in the liver and modulating HDL metabolism. Hepatitis C virus (HCV) is able to directly interact with SR-BI and requires this receptor to efficiently enter into hepatocytes to establish productive infection. A complex interplay between lipoproteins, SR-BI and HCV envelope glycoproteins has been reported to take place during this process. SR-BI has been demonstrated to act during binding and postbinding steps of HCV entry. Although the SR-BI determinants involved in HCV binding have been partially characterized, the postbinding function of SR-BI remains largely unknown. To uncover the mechanistic role of SR-BI in viral initiation and dissemination, we generated a novel class of anti-SR-BI monoclonal antibodies that interfere with postbinding steps during the HCV entry process without interfering with HCV particle binding to the target cell surface. Using the novel class of antibodies and cell lines expressing murine and human SR-BI, we demonstrate that the postbinding function of SR-BI is of key impact for both initiation of HCV infection and viral dissemination. Interestingly, this postbinding function of SR-BI appears to be unrelated to HDL interaction but to be directly linked to its lipid transfer function.
dc.language.isoenen
dc.rightsArchived with thanks to Hepatology (Baltimore, Md.)en_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshAntibodies, Monoclonalen_GB
dc.subject.meshAntigens, CD36en_GB
dc.subject.meshCell Lineen_GB
dc.subject.meshCholesterol, HDLen_GB
dc.subject.meshHepacivirusen_GB
dc.subject.meshHepatitis Cen_GB
dc.subject.meshHumansen_GB
dc.subject.meshLipoproteins, HDLen_GB
dc.subject.meshMiceen_GB
dc.subject.meshRatsen_GB
dc.subject.meshReceptors, Lipoproteinen_GB
dc.titleThe postbinding activity of scavenger receptor class B type I mediates initiation of hepatitis C virus infection and viral dissemination.en
dc.typeArticleen
dc.contributor.departmentINSERM, U748, Strasbourg, France.en_GB
dc.identifier.journalHepatology (Baltimore, Md.)en_GB
refterms.dateFOA2014-02-15T00:00:00Z
html.description.abstractScavenger receptor class B type I (SR-BI) is a high-density lipoprotein (HDL) receptor highly expressed in the liver and modulating HDL metabolism. Hepatitis C virus (HCV) is able to directly interact with SR-BI and requires this receptor to efficiently enter into hepatocytes to establish productive infection. A complex interplay between lipoproteins, SR-BI and HCV envelope glycoproteins has been reported to take place during this process. SR-BI has been demonstrated to act during binding and postbinding steps of HCV entry. Although the SR-BI determinants involved in HCV binding have been partially characterized, the postbinding function of SR-BI remains largely unknown. To uncover the mechanistic role of SR-BI in viral initiation and dissemination, we generated a novel class of anti-SR-BI monoclonal antibodies that interfere with postbinding steps during the HCV entry process without interfering with HCV particle binding to the target cell surface. Using the novel class of antibodies and cell lines expressing murine and human SR-BI, we demonstrate that the postbinding function of SR-BI is of key impact for both initiation of HCV infection and viral dissemination. Interestingly, this postbinding function of SR-BI appears to be unrelated to HDL interaction but to be directly linked to its lipid transfer function.


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