Key result
Nonsecretors were as likely to develop symptomatic norovirus gastroenteritis as secretors (OR 1.41), demonstrating a secretor-independent susceptibility pattern in this GI.3 outbreak.
Case-Control (n=83)
No
Odds Ratio: 1.41 (95% CI 0.46–4.36)
Absolute Event Rate: 47% vs 38%
p-value: p=0.57
This study demonstrates that a Norovirus GI.3 outbreak infected individuals regardless of their secretor status or Lewis/ABO phenotypes, challenging the previous understanding that nonsecretors are almost completely resistant to the disease.
May affect nonsecretors equally in GI.3 outbreaks; leaves open generalizability of secretor-independent susceptibility.
Norovirus (NoV) is recognized as the commonest cause of acute gastroenteritis among adults. Susceptibility to disease has been associated with histo-blood group antigens and secretor status; nonsecretors are almost completely resistant to disease. We report a foodborne outbreak of GI.3 NoV gastroenteritis that affected 33/83 (40%) persons. Symptomatic disease was as likely to develop in nonsecretors as in secretors (odds ratio [OR] 1.41, 95% confidence interval [CI] 0.46-4.36 vs. OR 0.71, 95% CI 0.23-2.18, p = 0.57). Moreover, no statistical difference in susceptibility was found between persons of different Lewis or ABO phenotypes. The capsid gene of the outbreak strain shares high amino acid homology with the Kashiwa645 GI.3 strain, previously shown to recognize nonsecretor saliva, as well as synthetic Lewis a. This norovirus outbreak affected persons regardless of secretor status or Lewis or ABO phenotypes.
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Nordgren et al. (2009) conducted a case-control in Norovirus gastroenteritis (n=83). Nonsecretor status vs. Secretor status was evaluated on Symptomatic norovirus infection (OR 1.41, 95% CI 0.46-4.36, p=0.57). Nonsecretors were as likely to develop symptomatic norovirus gastroenteritis as secretors (OR 1.41), demonstrating a secretor-independent susceptibility pattern in this GI.3 outbreak.
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