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Review
. 2021 Nov 2;17(11):4553-4566.
doi: 10.1080/21645515.2021.1961465. Epub 2021 Sep 8.

Epidemiology and evolution of Norovirus in China

Affiliations
Review

Epidemiology and evolution of Norovirus in China

Na Wei et al. Hum Vaccin Immunother. .

Abstract

Norovirus (NoV) has been recognized as a leading cause of gastroenteritis worldwide. This review estimates the prevalence and genotype distribution of NoV in China to provide a sound reference for vaccine development. Studies were searched up to October 2020 from CNKI database and inclusion criteria were study duration of at least one calendar year and population size of >100. The mean overall NoV prevalence in individuals with sporadic diarrhea/gastroenteritis was 16.68% (20796/124649, 95% CI 16.63-16.72), and the detection rate of NoV was the highest among children. Non-GII.4 strains have replaced GII.4 as the predominant caused multiple outbreaks since 2014. Especially the recombinant GII.P16-GII.2 increased sharply, and virologic data show that the polymerase GII.P16 rather than VP1 triggers pandemic. Due to genetic diversity and rapid evolution, predominant genotypes might change unexpectedly, which has become major obstacle for the development of effective NoV vaccines.

Keywords: China; Norovirus; epidemiology; evolution; genotype diversity; vaccine.

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Figures

Figure 1.
Figure 1.
Heat map of unique datasets from each province. The study references are as follow:Chongqing, Shaanxi,, Sichuan, Fujian,, Shanghai-,,,,, Jiangsu,,,, Guangxi,,, Qinghai,, InnerMongolia, Beijing,,, Guangdong,,,,,, Hubei, Shandong, Gansu,, Tianjin,,, Anhui,, Jilin, Ningxia,, Xinjiang,, Zhejiang,,,,,, Shanxi,, Hebei,, Yunnan, Heilongjiang,,, Hainan,, Hunan,, Liaoning,, Henan.
Figure 2.
Figure 2.
The predominant genotype of NoV in 1999–2019.,,,,,
Figure 3.
Figure 3.
(a) The Proportion of NoV Genotypes from 1999 to 2014 (1250 cases from 15 studies);,,,,,,,,,, (b)The Proportion of NoV Genotypes from 2014 to 2019 (1697 cases from 13 studies).,,,,,,,,
Figure 4.
Figure 4.
Summary of mutations in the P2 subdomain of GII.2 strains from 1970–2019 (Strains without mutations were not involved). Red letters denote concentrated mutations that have appeared in multiple sequences. GenBank accession numbers: ASO96884, AGI17590, AFN06726, AFX71659, AGT62523.
Figure 5.
Figure 5.
Phylogenetic analysis of GII.2 full length VP1 sequences. Minimum evolution method phylogenetic inference of VP1 aa sequences was performed. Statistical evaluation was performed by 1,000 bootstrap replications and percentages of clustering (>50%) are shown at nodes. Scale bars indicate the number of substitutions per site. Country/region abbreviations: CN, China (circles); JP, Japan (squares); US, United States (triangles); MY, Malaysia (diamonds); BJ, Beijing; TW, Taiwan; HK, Hong Kong; TZ, Taizhou; ZS, Zhoushan.
Figure 6.
Figure 6.
The hypothesis of recombination GII.P16-GII.2: GII.P16-GII.X positive-sense RNA as a template to synthesize negative-sense RNA. This negative-sense RNA and its internal subgenomic RNA are used as templates to synthesize positive-sense genomic RNA and subgenomic RNA respectively. These two positive-sense RNAs serve as template to synthetic negative-sense genomic RNA and subgenomic RNA. Recombination occurs during the process of synthesizing GII.P16-GII.X positive-sense RNA and subgenomic RNA. The RdRp region of the positive-sense RNA initiates synthesis at the promoter (blue triangle) located at the 3′end of negative-sense RNA. However, the process stalls at the ORF1/ORF2 overlap region subgenomic promoter (red triangle) and then switches template to GII.PX-GII.2 negative-sense subgenomic RNA to continue transcription and finally the recombinant strain GII.P16-GII.2 formed.

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Grants and funding

This review received no external funding.