Susceptibility to winter vomiting disease: a sweet matter
Article first published online: 25 AUG 2011
Copyright © 2011 John Wiley & Sons, Ltd.
Reviews in Medical Virology
Volume 21, Issue 6, pages 370–382, November 2011
How to Cite
Rydell, G. E., Kindberg, E., Larson, G. and Svensson, L. (2011), Susceptibility to winter vomiting disease: a sweet matter. Rev. Med. Virol., 21: 370–382. doi: 10.1002/rmv.704
- Issue published online: 25 OCT 2011
- Article first published online: 25 AUG 2011
- Manuscript Accepted: 23 JUN 2011
- Manuscript Revised: 21 JUN 2011
- Manuscript Received: 19 APR 2011
- Swedish Research Council. Grant Numbers: 10392 (LS) 8266 (GL), 2010-878 (GR)
- Sahlgrenska University Hospital (GL)
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. Copyright © 2011 John Wiley & Sons, Ltd.