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A FUT2 nonsense mut...
A FUT2 nonsense mutation (G428A) and Lewis-independent norovirus GI.3 outbreak
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- Nordgren, Johan, 1980- (författare)
- Linköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet
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- Kindberg, Elin (författare)
- Linköpings universitet,Molekylär virologi,Hälsouniversitetet
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- Lindgren, Per-Eric (författare)
- Linköpings universitet,Medicinsk mikrobiologi,Hälsouniversitetet
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- Matussek, Andreas (författare)
- Department of Clinical Microbiology, Division of Laboratory Medicine, County Hospital Ryhov, Jönköping, Sweden/Department of Clinical Microbiology, Capio Diagnostik AB, Capio St Görans Hospital, Stockholm, Sweden
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- Svensson, Lennart (författare)
- Linköpings universitet,Molekylär virologi,Hälsouniversitetet
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(creator_code:org_t)
- 2009
- 2009
- Engelska.
- Relaterad länk:
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http://urn.kb.se/res...
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https://urn.kb.se/re...
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Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- MEDICINE
- MEDICIN
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