Abstract
Norovirus (NoVs) are recognized as a leading cause of human gastroenteritis worldwide. Infection takes place following ingestion of contaminated food or most often through direct contact from person to person. However, not all individuals are equally sensitive to these viruses. Indeed, NoVs use ABH and Lewis glycans of the histo-blood group antigen family (HBGAs) as ligands. At the epithelial level synthesis of these HBGAs requires the action of several glycosyltransferases encoded by the ABO, FUT2 and FUT3 genes. Since the attachment profile to these glycans varies from strain to strain, the combined polymorphism at these three loci dictates sensitivity to NoV infection. Studies of the NoV-HBGA interactions together with phylogenetic analyses and the epidemiologic follow-up of strains indicate that NoVs transmission and evolution depends both on the establishment of herd immunity and on the genetic resistance of many individuals that contributes to restrict NoVs circulation, confering a herd innate proctection.
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