Genetic analyses of GII.17 norovirus strains in diarrheal disease outbreaks from December 2014 to March 2015 in Japan reveal a novel polymerase sequence and amino acid substitutions in the capsid region

Matsushima, Yuki; Ishikawa, Mariko; Shimizu, Tomomi; Komane, Ayako; Kasuo, Shizuko; Shinohara, Michiyo; Nagasawa, Kinzo; Kimura, Hirokazu; Ryo, Akihide; Okabe, Nobuhiko; Haga, Kei; Doan, Yen Hai; Katayama, Kazuhiko; Shimizu, Hideaki

doi:10.2807/1560-7917.es2015.20.26.21173

Cited by 174 publications

(138 citation statements)

References 11 publications

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“…GII.2 viruses were primarily associated with a GII.P2 polymerase, but GII.Pe-GII.2 and GII.P16-GII.2 were also detected. All GII.17 Kawasaki 308 viruses carried GII.P17 polymerases, which is consistent with strains reported widely in Asia (32,43). A GII.Pe-GII.17 virus sharing common ancestry with GII.17 viruses dating back to 1966 was also found (32).…”

Section: Discussionsupporting

confidence: 70%

Genetic and Epidemiologic Trends of Norovirus Outbreaks in the United States from 2013 to 2016 Demonstrated Emergence of Novel GII.4 Recombinant Viruses

et al. 2017

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Noroviruses are the most frequent cause of epidemic acute gastroenteritis in the United States. Between September 2013 and August 2016, 2,715 genotyped norovirus outbreaks were submitted to CaliciNet. GII.4 Sydney viruses caused 58% of the outbreaks during these years. A GII.4 Sydney virus with a novel GII.P16 polymerase emerged in November 2015, causing 60% of all GII.4 outbreaks in the 2015-2016 season. Several genotypes detected were associated with more than one polymerase type, including GI.3, GII.2, GII.3, GII.4 Sydney, GII.13, and GII.17, four of which harbored GII.P16 polymerases. GII.P16 polymerase sequences associated with GII.2 and GII.4 Sydney viruses were nearly identical, suggesting common ancestry. Other common genotypes, each causing 5 to 17% of outbreaks in a season, included GI.3, GI.5, GII.2, GII.3, GII.6, GII.13, and GII.17 Kawasaki 308. Acquisition of alternative RNA polymerases by recombination is an important mechanism for norovirus evolution and a phenomenon that was shown to occur more frequently than previously recognized in the United States. Continued molecular surveillance of noroviruses, including typing of both polymerase and capsid genes, is important for monitoring emerging strains in our continued efforts to reduce the overall burden of norovirus disease.

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Section: Discussionsupporting

confidence: 70%

Genetic and Epidemiologic Trends of Norovirus Outbreaks in the United States from 2013 to 2016 Demonstrated Emergence of Novel GII.4 Recombinant Viruses

et al. 2017

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“…2A) (17,38). NoV GII.17 strains detected in this study were classified as NA based on partial sequences of the RdRp region ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Detection of Enteric Viruses in Fecal Specimens from Nonbacterial Foodborne Gastroenteritis Outbreaks in Tokyo, Japan between 1966 and 1983

et al. 2017

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“…In the past decade, genogroup II genotype 4 (GII.4) norovirus strains were those mostly responsible for epidemic outbreaks (1)(2)(3). However, a GII.17 variant norovirus was found recently to cause an alarming number of outbreaks in certain parts of Asia in 2014 to 2015 (4)(5)(6)(7)(8). Before this time, the GII.17 norovirus was only a minor cause of infections, although it was first described in 1978 (9).…”

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confidence: 99%

Structural Evolution of the Emerging 2014-2015 GII.17 Noroviruses

Singh

Koromyslova

Hefele

et al. 2016

J Virol

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Recent reports suggest that human genogroup II genotype 17 (GII.17) noroviruses are increasing in prevalence. We analyzed the evolutionary changes of three GII.17 capsid protruding (P) domains. We found that the GII.17 P domains had little cross-reactivity with antisera raised against the dominant GII.4 strains. X-ray structural analysis of GII.17 P domains from 2002 to 2014 and 2015 suggested that surface-exposed substitutions on the uppermost part of the P domain might have generated a novel 2014-2015 GII.17 variant. Human noroviruses are the dominant cause of outbreaks of acute gastroenteritis. In the past decade, genogroup II genotype 4 (GII.4) norovirus strains were those mostly responsible for epidemic outbreaks (1-3). However, a GII.17 variant norovirus was found recently to cause an alarming number of outbreaks in certain parts of Asia in 2014 to 2015 (4-8). Before this time, the GII.17 norovirus was only a minor cause of infections, although it was first described in 1978 (9). Researchers are now reporting that the GII.17 variant is emerging in other parts of the world, and molecular epidemiologists have warned that the GII.17 norovirus might replace the predominant GII.4 norovirus (10).Noroviruses have a single-stranded, positive-sense RNA genome of 7.5 to 7.7 kb. The genome contains three open reading frames (ORFs). The first ORF (ORF1) encodes nonstructural proteins, including the RNA-dependent RNA polymerase (RdRp), ORF2 encodes capsid protein (VP1), and ORF3 encodes a minor capsid protein (VP2) (11). The X-ray crystal structure of the prototype (GI.1) virus-like particles (VLPs) identified two domains, the shell (S) domain and the protruding (P) domain, which can be further subdivided into P1 and P2 subdomains (12). The S domain surrounds the viral RNA, whereas the P domain contains the determinants for cell attachment and antigenicity. Human noroviruses are known to bind histo-blood group antigens (HBGAs), and the interaction is thought to be important for infection (13)(14)(15)(16). Two recent reports indicated that, similarly to other GII noroviruses, the recent GII.17 strains bind a panel of different HBGA types (4,8).Human noroviruses are believed to evolve in a manner similar to that seen with influenza viruses, where new norovirus genotype variants emerge every other year. Evolving strains with an ϳ5% amino acid change can reinfect the same individual (17). Data on short-and long-term immunity to human norovirus are still unclear, although vaccines are currently been tested in clinical trials (18,19). Unfortunately, the vaccines, which can include VLPs or P domains (20, 21), may not protect from antigenically divergent strains (18-21). Here, we report the first X-ray crystal structure of GII.17 norovirus P domains and describe the cross-reactivities with antibodies (Abs) raised against GII.4 strains, which are targeted by the current vaccines in clinical trials.Three different GII.17 norovirus strains were selected for antibody binding and structural analysis: a nonprevalent 2002 strain (Sai...

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Genetic analyses of GII.17 norovirus strains in diarrheal disease outbreaks from December 2014 to March 2015 in Japan reveal a novel polymerase sequence and amino acid substitutions in the capsid region

Cited by 174 publications

References 11 publications

Genetic and Epidemiologic Trends of Norovirus Outbreaks in the United States from 2013 to 2016 Demonstrated Emergence of Novel GII.4 Recombinant Viruses

Genetic and Epidemiologic Trends of Norovirus Outbreaks in the United States from 2013 to 2016 Demonstrated Emergence of Novel GII.4 Recombinant Viruses

Detection of Enteric Viruses in Fecal Specimens from Nonbacterial Foodborne Gastroenteritis Outbreaks in Tokyo, Japan between 1966 and 1983

Structural Evolution of the Emerging 2014-2015 GII.17 Noroviruses

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