Emergence of norovirus GII.P16-GII.2 strains in patients with acute gastroenteritis in Huzhou, China, 2016–2017

Han, Jae-Ik; Wu, Xiaofang; Chen, Liping; Fu, Yun Xin; Xu, Deshun; Zhang, Peng; Ji, Lei

doi:10.1186/s12879-018-3259-6

Cited by 28 publications

(26 citation statements)

References 33 publications

(43 reference statements)

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“…(Figure 5A,B). Particle integrity and carbohydrate binding profiles were screened for each of these mutants, and while the VLP were indistinguishable from the native GII.2 Chapel Hill strain via electron microscopy, all lost carbohydrate binding to both A and B saliva ( Figure 5C), supporting previous reports demonstrating that amino acids within the P2 domain are important for HBGA recognition [32,51]. To better understand residues on the GII.2 capsid that were important for mAb and HBGA recognition, a panel of 5 GII.2 Chapel Hill VLPs were designed with alanine mutations in regions where microvariation was observed between the prototypic 1976 and Chapel Hill GII.2 strains.…”

Section: Resultssupporting

confidence: 81%

Section: Resultssupporting

confidence: 81%

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Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains

Mallory

Lindesmith

Brewer-Jensen

et al. 2020

Viruses

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Human norovirus (HuNoV) is the leading cause of global infectious acute gastroenteritis, causing ~20% of reported diarrheal episodes. Typically, GII.4 strains cause 50–70% of yearly outbreaks, and pandemic waves of disease approximately every 2–7 years due to rapid evolution. Importantly, GII.4 dominance is occasionally challenged by the sudden emergence of other GII strains, most recently by GII.2 strains which peaked in 2016–2017, dramatically increasing from 1% to 20% of total HuNoV outbreaks. To determine if viral capsid evolution may account for the sudden rise in GII.2 outbreaks, Virus Like Particles (VLPs) of two 2016–2017 GII.2 strains were compared by antigenic and histo blood group antigen (HBGA) binding profiles to the prototypic 1976 GII.2 Snow Mountain Virus (SMV) strain. Despite >50 years of GII.2 strain persistence in human populations, limited sequence diversity and antigenic differences were identified between strains. However, capsid microvariation did affect HBGA binding patterns, with contemporary strains demonstrating decreased avidity for type A saliva. Furthermore, bile salts increased GII.2 VLP avidity for HBGAs, but did not alter antigenicity. These data indicate that large changes in antigenicity or receptor binding are unlikely to explain GII.2 emergence, in contrast to the pandemic GII.4 strains, and indicate that host factors such as waning or remodeling of serum or mucosal immunity likely contributed to the surge in GII.2 prevalence.

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Section: Resultssupporting

confidence: 81%

Section: Resultssupporting

confidence: 81%

Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains

Mallory

Lindesmith

Brewer-Jensen

et al. 2020

Viruses

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“…We found that GII.2[P16] viruses caused an increase in the number of norovirus outbreaks during winter 2016-17. The first GII.2[P16]positive sample was detected in August 2016 in Guangdong Province (36,37), and the number subsequently increased, with GII.2[P16] accounting for 70%-100% of norovirus outbreaks during winter 2016-17 in different provinces (38)(39)(40). Previous studies suggested that reemerging GII.2[P16] virus most likely evolved from strains emerging during 2012-2013 (41).…”

Section: Discussionmentioning

confidence: 99%

Norovirus Outbreak Surveillance, China, 2016–2018

Jin¹,

Wu²,

Kong³

et al. 2020

Emerg. Infect. Dis.

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H uman noroviruses are the leading cause of outbreaks of acute gastroenteritis, associated with ≈50% of all outbreaks worldwide (1). Norovirus outbreaks are frequently reported in semiclosed institutions, such as hospitals, nursing homes, schools, and childcare centers (2). The virus is primarily transmitted directly from person to person or indirectly through contaminated surfaces, food, or water (1). The relative stability of noroviruses on environmental surfaces makes infection control challenging (3). Several candidate norovirus vaccines are in clinical trials (4). Noroviruses are single-stranded RNA viruses that belong to the genus Norovirus, family Caliciviridae. The genome is organized into 3 open reading frames (ORFs): ORF1 encodes polyprotein, ORF2 encodes the major capsid protein (VP1), and ORF3 encodes the minor (VP2) capsid protein. The viruses are classified into at least 7 genogroups (G), of which viruses from GI, GII, and GIV infect humans (5,6). On the basis of the diversity of VP1, these genogroups can be further divided into at least 33 genotypes: 9 GI, 22 GII, and 2 GIV (7). In addition, on the basis of the diversity of the polymerase region of ORF1, >14 GI polymerase (GI.P) types and 27 GII.P types have been described (7). Because of the frequent recombination at the ORF1/ORF2 junction region, a dual-typing system has been proposed for GI and GII noroviruses (7). Since 2002, genogroup II, genotype 4 (GII.4), noroviruses have been associated with most norovirus outbreaks globally, and new GII.4 variants have emerged every 2-3 years (8). Monitoring the trends in the distribution of the various genotypes and possible association of certain strains with a more severe disease outcome is important for understanding and controlling norovirus epidemics (9). Several norovirus outbreak surveillance networks, including NoroNet (10) and CaliciNet (7,11), have been developed during the past decade. NoroNet captures molecular and epidemiologic data on norovirus outbreaks and sporadic cases submitted by 19 participating countries across Europe and Asia and by Australia. CaliciNet is a norovirus outbreak surveillance network in the United States in which state and local public health laboratories electronically submit laboratory data, including sequences from norovirus outbreaks, to a central database (https://www. cdc.gov/norovirus/reporting/calicinet/data.html). CaliciNet data are integrated with epidemiologic data

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“…The peak in this study was in December, when Shenzhen began to turn cold, and March, when temperature began to turn warm, which is suspected that climate changes have an impact on NoV transmission. The NoV outbreak usually occurs in hospitals, nursing homes, schools, child care centers, hotels and other semi-enclosed places [34][35][36]. A study in United States reported 3,960 NoV outbreaks between 2009 and 2013 and found that long-term care homes were the most frequent sites of NoV outbreaks [37].…”

Section: Hbga-binding Pro Le Epitopes Predicted and Epitope A To E Smentioning

confidence: 99%

Norovirus GII.P16/GII.2 Strain in Shenzhen, China: A Retrospective Study

Wang

Jin

Zhang

et al. 2020

Preprint

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Background Norovirus (NoV) is the main cause of non-bacterial acute gastroenteritis (AGE) outbreaks worldwide. From September 2015 through August 2018, 203 NoV outbreaks with 2,500 patients were reported to the Shenzhen Center for Disease Control and Prevention. Methods Fecal specimens were collected from the 203 outbreaks and epidemiological data were collected through the AGE outbreak surveillance system in Shenzhen. The genotypes were determined by sequencing analysis. To gain a better understanding of evolutionary characterization of NoV in Shenzhen, the molecular evolution was analyzed by time-scale evolutionary phylogeny and amino acid mutations. Results Most of these outbreaks were associated with NoV GII.P16/GII.2 strain (45.3%,92/203) and occurred in school settings (91.6%,186/203). The timescale phylogeny suggested that the GII.P16/GII.2 strain was recombination strain and were still stable. The amino acid mutations suggested that the nonstructural proteins of the recombination strain might play a more significant role than VP1 gene in these GII.P16/GII.2 recombination strain outbreaks. Conclusions This study illustrated the characteristics of the molecular epidemiological patterns in Shenzhen, China during September 2015 to August 2018 and provided the evidence that the GII.P16/GII.2 strain was static and the epidemic trend had fade.

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Emergence of norovirus GII.P16-GII.2 strains in patients with acute gastroenteritis in Huzhou, China, 2016–2017

Cited by 28 publications

References 33 publications

Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains

Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains

Norovirus Outbreak Surveillance, China, 2016–2018

Norovirus GII.P16/GII.2 Strain in Shenzhen, China: A Retrospective Study

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