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. 2010;2(3):117-126.
doi: 10.1007/s12560-010-9038-1.

Noroviruses - State of the Art

Affiliations

Noroviruses - State of the Art

Robert L Atmar. Food Environ Virol. 2010.

Abstract

Noroviruses are a common cause of both endemic and epidemic gastroenteritis. These highly infectious viruses usually cause self-limited disease, but chronic infections occur in highly immunocompromised patients and unusual manifestations are also being described in some populations. Histoblood-group antigen expression is now recognized as an important susceptibility factor for many norovirus strains, but a correlate of acquired immunity to infection or illness has not yet been identified. Currently, treatment and prevention strategies rely on non-specific measures. However, virus-like particles containing capsid antigens are undergoing evaluation as a vaccine candidate for illness prevention. This article reviews the biologic properties, epidemiology, clinical features, host susceptibility, diagnosis, and treatment and prevention of norovirus infection.

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Figures

Figure 1
Figure 1
Norovirus genomic organization and replication strategy. Norovirus is a positive strand RNA virus with three open reading frames (ORFs) encoding a large polyprotein from which non-structural proteins are produced by proteolytic cleavage and two structural proteins, VP1 and VP2. Replication takes place through a negative sense intermediate, from which the genomic RNA and a subgenomic RNA encoding the structural proteins are produced.
Figure 2
Figure 2
Classification of noroviruses into genogroups and genotypes. The Norovirus genus is divided into 5 genogroups (GI-GV). Each genogroup has from 1 to 19 different genotypes. GI.9 is a newly designated genotype, and its prototype strain is NoV/IF2036/2003/Iraq (AY675555).
Figure 3
Figure 3
Histoblood group synthetic pathway for blood group ABH and Lewis antigens. A type 1 precursor glycan is modified by fucosyltransferase-2 (FUT2) to produce the H type 1 glycan, which can be further modified by FUT3 (to produce Lewis-b [Leb]) and by A and B enzymes (enz) to produce the A and B histoblood group antigens (HBGAs). If FUT2 is non-functional, a person is a non-secretor, although the H type 1 precursor can still be modified to produce Lea in the presence of a functional FUT3. Persons with a functional FUT2 enzyme are called secretor positive because the ABH HBGAs are found in secretions and on mucosal surfaces.

References

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