Inhibition of the interaction between the SARS-CoV spike protein and its cellular receptor by anti-histo-blood group antibodies

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Title Inhibition of the interaction between the SARS-CoV spike protein and its cellular receptor by anti-histo-blood group antibodies
Author Guillon, Patrice Michel Guy; Clément, M.; Sébille, V.; Rivain, J-G.; Chou, C-F.; Pendu, J. Le
Journal Name Glycobiology
Year Published 2008
Place of publication Oxford, UK
Publisher Oxford University Press
Abstract Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic emergent virus which replicates in cells that can express ABH histo-blood group antigens. The heavily glycosylated SARS-CoV spike (S) protein binds to angiotensin-converting enzyme 2 which serves as a cellular receptor. Epidemiological analysis of a hospital outbreak in Hong Kong revealed that blood group O was associated with a low risk of infection. In this study, we used a cellular model of adhesion to investigate whether natural antibodies of the ABO system could block the S protein and angiotensin-converting enzyme 2 interaction. To this aim, a C-terminally EGFP-tagged S protein was expressed in chinese hamster ovary cells cotransfected with an alpha1,2-fucosyltransferase and an A-transferase in order to coexpress the S glycoprotein ectodomain and the A antigen at the cell surface. We observed that the S protein/angiotensin-converting enzyme 2-dependent adhesion of these cells to an angiotensin-converting enzyme 2 expressing cell line was specifically inhibited by either a monoclonal or human natural anti-A antibodies, indicating that these antibodies may block the interaction between the virus and its receptor, thereby providing protection. In order to more fully appreciate the potential effect of the ABO polymorphism on the epidemiology of SARS, we built a mathematical model of the virus transmission dynamics that takes into account the protective effect of ABO natural antibodies. The model indicated that the ABO polymorphism could contribute to substantially reduce the virus transmission, affecting both the number of infected individuals and the kinetics of the epidemic.
Peer Reviewed Yes
Published Yes
Alternative URI http://dx.doi.org/10.1093/glycob/cwn093
Volume 18
Issue Number 12
Page from 1085
Page to 1093
ISSN 0959-6658
Date Accessioned 2010-07-26
Language en_AU
Faculty Faculty of Science, Environment, Engineering and Technology
Subject Virology
URI http://hdl.handle.net/10072/38532
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1x

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