Skip Navigation


Glycobiology Advance Access originally published online on October 8, 2008
Glycobiology 2009 19(1):21-28; doi:10.1093/glycob/cwn098
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
19/1/21    most recent
cwn098v1
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

Association between expression of the H histo-blood group antigen, {alpha}1,2fucosyltransferases polymorphism of wild rabbits, and sensitivity to rabbit hemorrhagic disease virus

Patrice Guillon2, Nathalie Ruvoën-Clouet2,3, Béatrice Le Moullac-Vaidye2, Stéphane Marchandeau4 and Jacques Le Pendu1,2

2 INSERM, U892, Université de Nantes
3 Ecole Nationale Vétérinaire de Nantes
4 Office National de la Chasse et de la Faune Sauvage, Nantes, France

1 To whom correspondence should be addressed: Tel: +33-240-08-40-99; Fax: +33-240-08-40-82; e-mail: jlependu{at}nantes.inserm.fr

Received on August 21, 2008; revised on September 23, 2008; accepted on September 23, 2008

RHDV (rabbit hemorrhagic disease virus) is a highly virulent calicivirus that has become a major cause of mortality in wild rabbit populations (Oryctolagus cuniculus). It binds to the histo-blood group antigen (HBGA) H type 2 which requires an {alpha}1,2fucosyltransferase for its synthesis. In rabbit, three {alpha}1,2fucosyltransferases genes are known, Fut1, Fut2, and Sec1. Nonfunctional alleles at any of these loci could potentially confer resistance to RHDV, similar to human FUT2 alleles that determine the nonsecretor phenotype and resistance to infection by various NoV strains. In this study, we looked for the presence of H type 2 on buccal epithelial cells of wild rabbits from two geographic areas under RHDV pressure and from one RHDV-free area. Some animals with diminished H type 2 expression were found in the three populations (nonsecretor-like phenotype). Their frequency markedly increased according to the RHDV impact, suggesting that outbreaks selected survivors with low expression of the virus ligand. Polymorphisms of the Fut1, Fut2, and Sec1 coding regions were determined among animals that either died or survived outbreaks. The Fut2 and Sec1 genes presented a high polymorphism and the frequency of one Sec1 allele was significantly elevated, over 6-fold, among survivors. Sec1 enzyme variants showed either moderate, low, or undetectable catalytic activity, whereas all variant Fut2 enzymes showed strong catalytic activity. This functional analysis of the enzymes encoded by each Fut2 and Sec1 allele suggests that the association between one Sec1 allele and survival might be explained by a deficit of {alpha}1,2fucosyltransferase expression rather than by impaired catalytic activity.

Key words: fucosyltransferase / histo-blood group antigens / polymorphism / resistance to pathogens / RHDV


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.