A FUT2 nonsense mutation (G428A) and Lewis-independent norovirus GI.3 outbreak
2009 (English)Article in journal (Other academic) Submitted
Background: Norovirus (NoV) is recognized as the commonest cause of acute gastroenteritis among adults. Previous studies have shown that histo-blood group antigens (HBGAs) and secretor status are associated with susceptibility to symptomatic NoV infection, with non-secretors being almost completely resistant to disease. Here we report on a food-borne GI.3 NoV outbreak affecting 33/83 (40%) individuals.
Methods: Secretor status and HBGA expression in saliva were determined with pyrosequencing and ELISA. Virus characterization was performed by sequencing the N/S region and the complete capsid gene.
Results: A novel observation was that homozygous carriers of the nonsense FUT2 G428A allele were more susceptible to symptomatic infection than secretors (odds ratio [OR] 1.41 vs 0.71). Consistent with this observation was that Lewis a positive b negative (Lea+b-) individuals showed the highest susceptibility (OR 2.42) compared with other Lewis phenotypes. Blood group B was associated with partial protection (OR 0.27). The capsid gene of the outbreak strain exhibits high amino acid homology with the Kashiwa645 GI.3 strain, previously shown to recognize non-secretor saliva.
Conclusion: We describe for the first time a NoV outbreak with Lea+b- individuals homozygous for the G428A nonsense mutation in the FUT2 gene being more susceptible for disease than secretor-positive individuals.
Place, publisher, year, edition, pages
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-17686OAI: oai:DiVA.org:liu-17686DiVA: diva2:211304