[Noroviruses--tactic of spread]

Noroviruses are the commonest cause of nonbacterial acute gastroenteritis worldwide. Food and water are considered as the main source of the food-borne infections in humans. Noroviruses outbreaks are frequently associated with semiclosed or closed institutions such as hospitals, homes for the elderly, schools. Transmission of noroviruses is usually person-to-person, although food and environmental or airborne contamination have all been implicated in transmission and are members of the Caliciviridae family. The genomic diversity noroviruses includes 5 genogroups (GI-GV). Diversity among noroviruses is maintained through the accumulation of point mutations associated with nature RNA replication and genetic recombination involving the exchange of sequence between two related RINA viruses. The evolutionary mechanisms governing the persistence and emergence of new norovirus strains in human populations are unknown. The majority of norovirus outbreaks are caused by viruses from the GII.4 genoclusters, which was first recognized as the major epidemic strain in the mid-1990s. Some noroviruses readily infect humans who carry a gene encoding a alpha-1,2-fucosyltransferase (FUT2) and they express ABH histo-blood group antigens (HBGAs), a highly heterogeneous group of related carbohydrates on mucosal surface. Individuals with defects in the FUT2 are resistant to Norwalk virus infection. Surface-exposed carbohydrate ligand binding domain in the norovirus capsid is under heavy immune selection and likely evolves by antigenic drift in the face of human herd immunity. Variation in the capsid carbohydrate-binding domain is tolerated because of the large repertoire of similar, yet distinct HBGA carbohydrate receptors available on mucosal surfaces that could interface with the remodeled architecture of the capsid ligand-binding pocket.