Increase in genogroup II.4 norovirus host spectrum by CagA-positive Helicobacter pylori infection.

BACKGROUND:Noroviruses (NoVs) represent a considerable public health burden. Despite their enormous genetic diversity, most outbreaks are due to the single GII.4 genotype, but the reasons for this are poorly understood. NoVs use histo-blood group antigens (HBGAs) as attachment factors. Since HBGAs are present in saliva, binding of strains to saliva is commonly used as a surrogate for recognition of the gut surface by specific strains, although the relationship between saliva and gut tissue expression of HBGAs is not well defined. METHODS:The presence of fucosylated HBGAs in saliva and stomach biopsy specimens, as well as that of genogroup I.1 and genogroup II.4 virus-like particles, were compared in a series of 109 donors from Portugal. RESULTS:An overall good concordance between HBGA expression in saliva and stomach surface mucosa was observed. However, unexpected mucosal expression of α(1,2)fucosylated epitopes in nonsecretor individuals was frequently detected, allowing for GII.4 attachment. Although all individuals were infected with Helicobacter pylori, abnormal expression of α(1,2)fucosylated motifs and binding of GII.4 virus-like particles in nonsecretors' mucosa were associated with positivity for the H. pylori CagA virulence factor. CONCLUSIONS:Infection by CagA-positive H. pylori induces expression of GII.4 attachment factors in nonsecretors' mucosa, expanding the host range of these strains and thereby possibly contributing to their epidemiological dominance.