Dataset Information

Two gastroenteritis outbreaks caused by GII Noroviruses: host susceptibility and HBGA phenotypes.

ABSTRACT: Noroviruses (NoVs) cause epidemic acute gastroenteritis, in which histo-blood group antigens (HBGAs) may play an important role in the host susceptibility. To further explore this issue, two outbreaks of acute gastroenteritis caused by a GII.4 and a GII.3 NoV, respectively, in China in 2009 were studied. Stool and saliva samples from symptomatic patients and water samples from the outbreak facilities were collected. RT-PCR showed that 23 out of 33 (GII.4 outbreak) and 12 out of 13 (GII.3outbreak) stool samples were NoV positive. For the GII.4 outbreak the NoV sequences of stool and water samples were from an identical GII.4 strain, while the same GII.3 NoV sequences were found in five stool samples from the GII.3 outbreak. The HBGA phenotypes (A, B, Le(a), Le(b), Le(x), and Le(y)) of all saliva samples were determined, which revealed both secretors and nonsecretors in the symptomatic groups of the two outbreaks. In the GII.3 outbreak, type O individuals appeared less susceptible, while the type A may be more at risk of infection. However, No preference of HBGAs was observed in the GII.4 outbreak. The observation that nonsecretors were infected in both outbreaks differed from the previous results that nonsecretors are resistant to these two GII NoVs.

SUBMITTER: Jin M

PROVIDER: S-EPMC3589376 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Two gastroenteritis outbreaks caused by GII Noroviruses: host susceptibility and HBGA phenotypes.

Jin Miao M He Yaqing Y Li Huiying H Huang Pengwei P Zhong Weiming W Yang Hong H Zhang Hailong H Tan Ming M Duan Zhao-jun ZJ

PloS one 20130305 3

Noroviruses (NoVs) cause epidemic acute gastroenteritis, in which histo-blood group antigens (HBGAs) may play an important role in the host susceptibility. To further explore this issue, two outbreaks of acute gastroenteritis caused by a GII.4 and a GII.3 NoV, respectively, in China in 2009 were studied. Stool and saliva samples from symptomatic patients and water samples from the outbreak facilities were collected. RT-PCR showed that 23 out of 33 (GII.4 outbreak) and 12 out of 13 (GII.3outbreak ...[more]

PMID: 23472212

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Project description:Genogroup II, genotype 4 (GII.4) noroviruses are known to rapidly evolve, with the emergence of a new primary strain every 2 to 4 years as herd immunity to the previously circulating strain is overcome. Because viral genetic diversity is higher in chronic than in acute infection, chronically infected immunocompromised people have been hypothesized to be a potential source for new epidemic GII.4 strains. However, while some capsid protein residues are under positive selection and undergo patterned changes in sequence variation over time, the relationships between genetic variation and antigenic variation remains unknown. Based on previously published GII.4 strains from a chronically infected individual, we synthetically reconstructed virus-like particles (VLPs) representing early and late isolates from a small-bowel transplant patient chronically infected with norovirus, as well as the parental GII.4-2006b strain. We demonstrate that intrahost GII.4 evolution results in the emergence of antigenically distinct strains over time, comparable to the variation noted between the chronologically predominant GII.4 strains GII.4-2006b and GII.4-2009. Our data suggest that in some individuals the evolution that occurs during a chronic norovirus infection overlaps with changing antigenic epitopes that are associated with successive outbreak strains and may select for isolates that are potentially able to escape herd immunity from earlier isolates.Noroviruses are agents of gastrointestinal illness, infecting an estimated 21 million people per year in the United States alone. In healthy individuals, symptomatic infection typically resolves within 24 to 48 h. However, symptoms may persist for years in immunocompromised individuals, and development of successful treatments for these patients is a continuing challenge. This work is relevant to the design of successful norovirus therapeutics for chronically infected patients; provides support for previous assertions that chronically infected individuals may serve as reservoirs for new, antigenically unique emergent strains; and furthers our understanding of genogroup II, genotype 4 (GII.4) norovirus immune-driven molecular evolution.

Project description:Human noroviruses (huNoVs) cause epidemic acute gastroenteritis using histo-blood group antigens (HBGAs) as host receptors or attachment factors to initiate an infection. While most huNoVs have been shown to bind HBGAs, some known clinical isolates, such as GI.3 DSV and VA115, do not recognize any HBGAs and thus the molecular mechanism behind their infections remains elusive. In this study, we provided both phenotypic and structural evidence to show that huNoV DSV and VA115 recognize a group of glycans with terminal galactoses as ligands. First, through glycan array we found that both DSV and VA115 protruding (P) domain proteins bound two oligosaccharides that share common terminal galactoses. Then, by determination of the crystal structures of DSV/VA115 P proteins in complex with Galα1-3Galβ1-4Glc and/or NA2 N-Glycan, respectively, we showed that the terminal galactose is the main saccharide recognized by the two viral proteins. Our data demonstrated that GI huNoVs can interact with non-HBGA glycans through their conserved galactose binding site, shedding light on the mechanism of huNoV adaptation through recognizing new glycan receptors to facilitate their widespread nature in human population. These findings are also of significance in strategy development for huNoV control and prevention, as well as development of antiviral drugs. IMPORTANCE Human noroviruses (huNoVs) are the most important viral pathogens causing epidemic acute gastroenteritis worldwide. Previous studies indicated that histo-blood group antigens (HBGAs) are critical host-susceptibility factors affecting huNoV host susceptibility, host range, and probably prevalence. However, certain huNoVs, such as GI.3 DSV and VA115, do not recognize any HBGAs. This implies that other unknown host factors might exist and the molecular mechanism underlying their host receptor recognition or attachment remains elusive. In this study, we found that purified capsid protruding domain proteins from two GI.3 huNoVs specifically bind two glycans that contain a common terminal galactose. We solved the crystal structures of the complexes at atomic resolution and validated the vital amino acids involved in glycan recognition. Our findings elucidate the mechanism of GI.3 huNoV-non-HBGA glycan interaction, which explains why GI.3 virus strains could not bind human HBGAs, paving a way to the prevention and treatment of huNoV-associated diseases.

Dataset Information

Two gastroenteritis outbreaks caused by GII Noroviruses: host susceptibility and HBGA phenotypes.

Publications

Two gastroenteritis outbreaks caused by GII Noroviruses: host susceptibility and HBGA phenotypes.

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