Emergence of the GII-4 Norovirus Sydney2012 Strain in England, Winter 2012–2013

Allen, David J.; Adams, Natalie; Aladin, Farah; Harris, John P.; Brown, David

doi:10.1371/journal.pone.0088978

Cited by 33 publications

(34 citation statements)

References 27 publications

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“…Amino acid position 373 exhibited an N373H change between P.D1 and P.D302 but was conserved in major GII.4 epidemic strains until an N373R substitution emerged in GII.4-2012 Sydney. Although not supported with empirical data, recent work by Allen et al (43) suggests that this change in the Sydney strain may have impacted its emergence. Since changes to residue 373 have never been shown to influence immunogenicity, and it is not included as a diagnostic A epitope site residue, this potentially hampers new epidemic strain identification.…”

Section: Table 2 Gii4 Mouse and Human Mab Eia Reactivities With Chromentioning

confidence: 95%

Within-Host Evolution Results in Antigenically Distinct GII.4 Noroviruses

Debbink

Lindesmith

Ferris

et al. 2014

J Virol

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Genogroup II, genotype 4 (GII.4) noroviruses are known to rapidly evolve, with the emergence of a new primary strain every 2 to 4 years as herd immunity to the previously circulating strain is overcome. Because viral genetic diversity is higher in chronic than in acute infection, chronically infected immunocompromised people have been hypothesized to be a potential source for new epidemic GII.4 strains. However, while some capsid protein residues are under positive selection and undergo patterned changes in sequence variation over time, the relationships between genetic variation and antigenic variation remains unknown. Based on previously published GII.4 strains from a chronically infected individual, we synthetically reconstructed virus-like particles (VLPs) representing early and late isolates from a small-bowel transplant patient chronically infected with norovirus, as well as the parental GII.4-2006b strain. We demonstrate that intrahost GII.4 evolution results in the emergence of antigenically distinct strains over time, comparable to the variation noted between the chronologically predominant GII.4 strains GII.4-2006b and GII.4-2009. Our data suggest that in some individuals the evolution that occurs during a chronic norovirus infection overlaps with changing antigenic epitopes that are associated with successive outbreak strains and may select for isolates that are potentially able to escape herd immunity from earlier isolates. IMPORTANCENoroviruses are agents of gastrointestinal illness, infecting an estimated 21 million people per year in the United States alone. In healthy individuals, symptomatic infection typically resolves within 24 to 48 h. However, symptoms may persist for years in immunocompromised individuals, and development of successful treatments for these patients is a continuing challenge. This work is relevant to the design of successful norovirus therapeutics for chronically infected patients; provides support for previous assertions that chronically infected individuals may serve as reservoirs for new, antigenically unique emergent strains; and furthers our understanding of genogroup II, genotype 4 (GII.4) norovirus immune-driven molecular evolution.

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Section: Table 2 Gii4 Mouse and Human Mab Eia Reactivities With Chromentioning

confidence: 95%

Within-Host Evolution Results in Antigenically Distinct GII.4 Noroviruses

Debbink

Lindesmith

Ferris

et al. 2014

J Virol

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“…Several global epidemics caused by different GII.4 variants in the winter season have been reported, including those that arose during the winter season of 1995/96 (caused by the 95/96 US variant), 2002/03 (caused by the Farmington Hills variant), 2004/06 (caused by the Hunter variant), 2006/07 (caused by the 2006b variant), and 2008/09 (caused by the New Orleans variant) [1,26,4,28,13]. The Sydney 2012 variant was first identified in Australia in March 2012, which had become global by late 2012 [30–35]. In the United States, the GII.4 Sydney variant caused a total of 141 (53%) of the 266 NoV outbreaks recorded from September to December of 2012 [48].…”

Section: Discussionmentioning

confidence: 99%

“…In Denmark, GII.4 Sydney accounted for 46 of the 106 (43%) NoV-positive samples typed from both surveillance and outbreaks from October to December of 2012 [49]. An increase in epidemics associated with the emergence of GII.4 Sydney was also reported in the UK, France, Japan, Australia, New Zealand by late 2012 [30–35,43]. …”

Section: Discussionmentioning

confidence: 99%

“…New variants tend to emerge from and supersede the then-predominant GII.4 variant every 2–3 years [24]. Several GII.4 variants have been attributed to numerous NoV gastroenteritis pandemics from 1996 to present, including the outbreaks of 95/96 US (1995–96) [25,4], Farmington Hills (2002–03) [13], Hunter (2004–05)[1], 2006b (2006–07) [26,27], New Orleans (2009–10) [28,29], and the most recent variant of Sydney 2012 (2012–13) [30–35]. Other GII.4 variants have caused regional epidemics—namely Henry 2001, Japan 2001, Asia 2003, 2006a, and Abeldoorn 2008 [36,24,37–42].…”

Section: Introductionmentioning

confidence: 99%

“…The recently emerged GII.4 variant, Sydney 2012, was firstly identified in Australia early in 2012, but also lead the increase of acute gastroenteritis outbreaks in the United States, France, Japan, United Kingdom, the Netherlands, New Zealand, and Hong Kong [30–35,43]. Furthermore, the Sydney 2012 variant was also responsible for three gastroenteritis outbreaks in two social welfare homes and a factory in Shenzhen, China, in 2012/13.…”

Section: Introductionmentioning

confidence: 99%

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Gastroenteritis Outbreaks Associated with the Emergence of the New GII.4 Sydney Norovirus Variant during the Epidemic of 2012/13 in Shenzhen City, China

Jin

Chen

et al. 2016

PLoS ONE

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Noroviruses (NoVs) are the leading cause of gastroenteritis outbreaks in humans worldwide. Since late 2012, a new GII.4 variant Sydney 2012 has caused a significant increase in NoV epidemics in several countries. From November of 2012 to January of 2013, three gastroenteritis outbreaks occurred in two social welfare homes (Outbreaks A and B) and a factory (Outbreak C) in Shenzhen city of China. Feces and swabs were collected for laboratory tests for causative agents. While no bacterial pathogen was identified, all three outbreaks were caused by NoVs with detection rates of 26.2% (16/61) at Outbreak A, 35.2% (38/108) at Outbreak B), and 59.3% (16/27) at Outbreaks C. For Outbreak B, 25 of the 29 symptomatic individuals (86.2%) and 13 of the 79 asymptomatic individuals (16.5%) were found NoV-positive. For Outbreak C, an asymptomatic food handler was NoV-positive. All thirteen NoV sequences from the three outbreaks were classified into genogroup II and genotype 4 (GII.4), which we identified to be the GII.4 Sydney 2012 variant. The genome of two isolates from Outbreaks A and B were recombinant with the opening reading frame (ORF) 1 of GII.4 Osaka 2007 and ORF2 and 3 of the GII.4 New Orleans. Our study indicated that the GII.4 Sydney 2012 variant emerged and caused the outbreaks in China.

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Molecular epidemiology of genogroup II norovirus infection among hospitalized children with acute gastroenteritis in Suzhou (Jiangsu, China) from 2010 to 2013

Zhang³

et al. 2015

Journal of Medical Virology

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Noroviruses (NoVs) are the most common cause of acute gastroenteritis in both sporadic and outbreak cases. Genotyping and recombination analyses were performed in order to help getting more knowledge of the distribution and genetic diversity of NoVs in Suzhou, located in Jiangsu province of China. All stool samples were collected from hospitalized children younger than 5 years old with acute gastroenteritis. For genotyping, the open reading frame (ORF) 1 and ORF2 were partially amplified and sequenced. 26.9% of stool samples were positive for genogroup II NoVs. The most common genotype was GII.4 and its variants included Den Haag-2006b, New Orleans-2009, and Sydney-2012. The Den Haag-2006b variants predominated during 2010-2012. In 2013, it was replaced by the Sydney-2012 variant. The second most common genotype was GII.12/GII.3. NoVs could be detected throughout the year, with GII.4 and GII.12/GII.3 coexisting during the cold months, and GII.4 was the main genotype during the warm months. The highest prevalence of NoV was detected in young children aged <24 months. Patients infected with GII.4 had a higher chance of getting moderate fever than other NoV-positive patients, while those infected with GII.12/GII.3 tended to have a mild degree of fever. NoV is an important pathogen responsible for viral gastroenteritis among children in Suzhou. Analyses of NoV circulating between 2010 and 2013 revealed a change of predominant variant of NoV GII.4 in each epidemic season and intergenotype recombinant strains represented an important part.

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Emergence of the GII-4 Norovirus Sydney2012 Strain in England, Winter 2012–2013

Cited by 33 publications

References 27 publications

Within-Host Evolution Results in Antigenically Distinct GII.4 Noroviruses

Within-Host Evolution Results in Antigenically Distinct GII.4 Noroviruses

Gastroenteritis Outbreaks Associated with the Emergence of the New GII.4 Sydney Norovirus Variant during the Epidemic of 2012/13 in Shenzhen City, China

Molecular epidemiology of genogroup II norovirus infection among hospitalized children with acute gastroenteritis in Suzhou (Jiangsu, China) from 2010 to 2013

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