Abstract
In the winter of 2014/15 a novel GII.P17-GII.17 norovirus strain (GII.17 Kawasaki 2014) emerged, as a major cause of gastroenteritis outbreaks in China and Japan. Since their emergence these novel GII.P17-GII.17 viruses have replaced the previously dominant GII.4 genotype Sydney 2012 variant in some areas in Asia but were only detected in a limited number of cases on other continents. This perspective provides an overview of the available information on GII.17 viruses in order to gain insight in the viral and host characteristics of this norovirus genotype. We further discuss the emergence of this novel GII.P17-GII.17 norovirus in context of current knowledge on the epidemiology of noroviruses. It remains to be seen if the currently dominant norovirus strain GII.4 Sydney 2012 will be replaced in other parts of the world. Nevertheless, the public health community and surveillance systems need to be prepared in case of a potential increase of norovirus activity in the next seasons caused by this novel GII.P17-GII.17 norovirus.
Highlights
In the winter of 2014/15 a novel GII.P17-GII.17 norovirus strain (GII.17 Kawasaki 2014) emerged, as a major cause of gastroenteritis outbreaks in China and Japan
In this issue of Eurosurveillance, observations from Japan are reported on an unusual prevalence of a previously rare norovirus genotype, GII.17, in diarrheal disease outbreaks at the end of the 2014/15 winter season [1], similar to what was observed for China [2,3]
AGE: acute gastroenteritis; HIV: human immunodeficiency virus; NCBI: National Center for Biotechnology Information; ORF: open reading frame. a GII.17 detection location with study location between brackets. b GII.17 detection year(s) with study years between brackets. c Either the proportion of strains that was typed as GII.17 or the proportion of outbreaks that was caused by GII.17 is given. d Information derived from the GenBank entry related to the accession number of the sequence
Summary
AGE: acute gastroenteritis; HIV: human immunodeficiency virus; NCBI: National Center for Biotechnology Information; ORF: open reading frame. a GII. detection location with study location between brackets (when different from GII. detection location). b GII. detection year(s) with study years between brackets. c Either the proportion of strains that was typed as GII. or the proportion of outbreaks that was caused by GII. is given. d Information derived from the GenBank entry related to the accession number of the sequence. For only a limited number of GII. strains the full VP1 has been sequenced, which demonstrated three deletions and at least one insertion compared with previous GII. strains (comprehensive alignments are given in Fu et al and Parra et al [2,21]) The majority of these changes could be mapped in or near major epitopes of the VP1 protein and potentially result in antigenic drift or altered receptor-binding properties [21]. In studies investigating the genetic susceptibility to norovirus genotypes, a secretor patient with blood type O Lewis phenotype Lea-b + and a secretor patient with blood type B Lewis phenotype Lea-b- were positive for previously identified GII. viruses and no non-secretors were found positive [26,27], suggesting that there could be genetic restrictions for GII. viruses in infection of humans. How the observed genetic changes have affected the antigenic and binding properties of the novel GII. strains, and hereby the susceptible host population, remains to be discovered
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