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Susceptibility to winter vomiting disease: a sweet matter.

Review article
Authors Gustaf E Rydell
Elin Kindberg
Göran Larson
Lennart Svensson
Published in Reviews in medical virology
Volume 21
Issue 6
Pages 370-82
ISSN 1099-1654
Publication year 2011
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Pages 370-82
Language en
Links dx.doi.org/10.1002/rmv.704
Subject categories Virology, Clinical chemistry, Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)

Abstract

Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200,000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease.

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