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<p>Noroviruses are the primary viral pathogens responsible for epidemic acute gastroenteritis. The novel GII.4 Sydney 2012 variant, which emerged during the 2012/13 winter season, led to significant global outbreaks. This study reports large-scale outbreaks occurring in the university town of Guangzhou, China, from January 8 to April 3, 2013. These outbreaks affected 652 individuals across five universities and one middle school. Of the 386 samples tested, 114 were norovirus-positive, and 19 stool or swab samples were genotyped as the GII.4 Sydney 2012 strain. The genome sequence of the GII.4 Sydney 2012 variant, GZ3135, was determined and compared with those of earlier GII.4 variants. This comparison revealed residue substitutions at specific sites, including the HBGA binding pocket and putative antigenic epitopes. The investigation outcomes showed that GII.4 Sydney variant infected individuals with both secretor and nonsecretor phenotypes. This finding was consistent with the HBGA binding results that the recombinant P protein of the GII.4 Sydney variant bound to saliva samples of nonsecretors, as well as the Lewis x and Lewis a oligosaccharides. Taken together, our data suggested that the GII.4 Sydney 2012 variant gained new HBGA binding ability and antigenic features which may contribute to its widespread epidemics.</p>

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Large-scale gastroenteritis outbreaks occurring in a university town of Guangzhou city during the global wave of the norovirus in China

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月19日

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  • Yi Tian,
  • Jun Yuan,
  • Wenfeng Cai,
  • Huaping Xie,
  • Yanhui Yang,
  • Lijiao Cao,
  • Shi Cong,
  • Xiangyu Kong,
  • Qing Zhang,
  • Miao Jin

摘要

Noroviruses are the primary viral pathogens responsible for epidemic acute gastroenteritis. The novel GII.4 Sydney 2012 variant, which emerged during the 2012/13 winter season, led to significant global outbreaks. This study reports large-scale outbreaks occurring in the university town of Guangzhou, China, from January 8 to April 3, 2013. These outbreaks affected 652 individuals across five universities and one middle school. Of the 386 samples tested, 114 were norovirus-positive, and 19 stool or swab samples were genotyped as the GII.4 Sydney 2012 strain. The genome sequence of the GII.4 Sydney 2012 variant, GZ3135, was determined and compared with those of earlier GII.4 variants. This comparison revealed residue substitutions at specific sites, including the HBGA binding pocket and putative antigenic epitopes. The investigation outcomes showed that GII.4 Sydney variant infected individuals with both secretor and nonsecretor phenotypes. This finding was consistent with the HBGA binding results that the recombinant P protein of the GII.4 Sydney variant bound to saliva samples of nonsecretors, as well as the Lewis x and Lewis a oligosaccharides. Taken together, our data suggested that the GII.4 Sydney 2012 variant gained new HBGA binding ability and antigenic features which may contribute to its widespread epidemics.