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Norovirus Immunity and the Great Escape

Figure 1

NoV Genetic Diversity, Structure, and Binding Ligand.

1A: NoV genome schematic. The NoV genome encodes three open reading frames. ORF 1 encodes the nonstructural proteins (blue); ORF 2 encodes VP1, the major capsid protein (purple); and ORF 3 encodes VP2, the minor capsid protein (green). VP1 is further divided into the shell, which forms the base of the virion (teal); the P1 subdomain, which forms a stalk-like projection from the surface (orange); and the P2 subdomain, which is the most variable and surface-exposed area of the virion, contains ligand binding sites, and interacts with potentially neutralizing antibodies (red). 1B: NoV phylogenetic tree. NoVs are divided into five genogroups. Genogroups 1 (pink) and 2 (orange) cause the majority of human disease. Genogroups are further divided into genotypes. Genotype GII.4 NoVs (red bracket) account for ∼80% of outbreaks. Genotype GI.1 NoVs are the prototypic Norwalk viruses. 1C: NoV capsid protein (VP1) cryo EM image. Colors correspond approximately to the shell (teal), the P1 subdomain (yellow/orange) and the P2 subdomain (red). 1D. Secretor/non-secretor phenotype pathways. Enzymes (Secretor or Lewis) add specific modifications to a precursor molecule. Individuals without a functional FUT2 gene cannot express HBGAs from the left branch of the pathway (left of the dotted line) on mucosal surfaces. For those without a functional FUT2 gene (non-secretors), the precursor molecule can still be modified by the Lewis enzyme to make Lewis a antigen (branch on the right side of the dotted line).

Figure 1

doi: https://doi.org/10.1371/journal.ppat.1002921.g001