Skip Navigation



Glycobiology Advance Access published online on September 25, 2008
Glycobiology, doi:10.1093/glycob/cwn093
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
18/12/1085    most recent
cwn093v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Guillon, P.
Right arrow Articles by Le Pendu, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Guillon, P.
Right arrow Articles by Le Pendu, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

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

Patrice Guillon2,3, Monique Clément2,3, Véronique Sébille4, Jean-Gérard Rivain4, Chih-Fong Chou5, Nathalie Ruvoën-Clouet3,6 and Jacques Le Pendu1,3

3 INSERM, U892, Nantes, France; University of Nantes, Nantes, France
4 EA 4275, University of Nantes, Nantes, France
5 Institute of Molecular and Cell Biology, Singapore
6 Ecole Nationale Vétérinaire de Nantes, Nantes, France

1 To whom correspondence should be addressed INSERM U892, Institut de Biologie, 9 Quai Moncousu, 44093, Nantes Cedex 01, France, Tel: 33 240 08 40 99, Fax: 33 240 08 40 82, E-mail: jlependu{at}nantes.inserm.fr

Received on June 4, 2008; accepted on September 22, 2008

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 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 {alpha}1,2fucosyltransferase 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.

Key words: SARS / histo-blood group antigens / natural antibodies / ABO / cellular receptor

2 These two authors contributed equally to the work

One supplementary material file is provided


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.