ArticleBMC infectious diseases2021
Norovirus GII.2[P16] strain in Shenzhen, China: a retrospective study.
Article in BMC infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Molecular Epidemiology of Norovirus Outbreaks in Childcare Centers and Schools in South Korea in 2023.Journal of microbiology and biotechnology · 2025Article
- Biological and immunological characterization of major capsid protein VP1 from distinct GII.2 norovirus clusters.Scientific reports · 2024Article
- Changing predominance of norovirus strains in children with acute gastroenteritis in Shanghai, 2018-2021.Virologica Sinica · 2023Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundNorovirus (NoV) is the main cause of non-bacterial acute gastroenteritis (AGE) outbreaks worldwide. From September 2015 through August 2018, 203 NoV outbreaks involving 2500 cases were reported to the Shenzhen Center for Disease Control and Prevention.
methodsFaecal specimens for 203 outbreaks were collected and epidemiological data were obtained through the AGE outbreak surveillance system in Shenzhen. Genotypes were determined by sequencing analysis. To gain a better understanding of the evolutionary characteristics of NoV in Shenzhen, molecular evolution and mutations were evaluated based on time-scale evolutionary phylogeny and amino acid mutations.
resultsA total of nine districts reported NoV outbreaks and the reported NoV outbreaks peaked from November to March. Among the 203 NoV outbreaks, 150 were sequenced successfully. Most of these outbreaks were associated with the NoV GII.2[P16] strain (45.3%, 92/203) and occurred in school settings (91.6%, 186/203). The evolutionary rates of the RdRp region and the VP1 sequence were 2.1 × 10
conclusionsThis study illustrates the molecular epidemiological patterns in Shenzhen, China, from September 2015 to August 2018 and provides evidence that the epidemic trend of GII.2[P16] recombinant strain had weakened and the non-structural proteins of the recombinant strain might have played a more significant role than VP1.
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