Rapid emergence of novel GII.4 sub-lineages noroviruses associated with outbreaks in Huzhou, China, 2008-2012.
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SUBMITTER: Ji L
PROVIDER: S-EPMC3853588 | biostudies-literature | 2013
REPOSITORIES: biostudies-literature
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Project description:BackgroundNorovirus (NoV) has been recognized as the leading cause of both outbreaks and sporadic cases of acute gastroenteritis in children and adults worldwide. Stool samples collected from outpatients with clinical symptoms of acute gastroenteritis in all age groups at the First People's Hospital in Huzhou, Huzhou, China between March 2014 and February 2015 were analyzed to gain insight into the epidemiology and genetic variation in NoV strains circulating in China.MethodReal-time RT-PCR (qPCR) was performed for Norovirus detection. RT-PCR were used for genomic amplification and sequencing. Genogroup and genotype were assigned using the NoV Noronet typing tool and the strains were named according to the time of isolation. The phylogenetic analysis was conducted using MEGA 5.ResultsOf the 809 specimens, 193 (23.9 %) were positive for NoV, with GII.4 and GII.17 the most commonly identified strains. Phylogenetic analysis confirmed the presence of five recombinant strains in Huzhou. Recombinants GII.P13/GII.17 and GII.P12/GII.4 were newly detected in China. The GII.P13/GII.17 recombinant was first identified in October 2014 and steadily replaced GII.Pe/GII.4 (GII.4 Sydney 2012) as the predominant circulating NoV genotype.ConclusionThis is the first report of the detection of GII.17 in the Huzhou area and of a NoV genotype being detected in greater numbers than GII.4. Furthermore, our results indicated that following the emergence of GII.17 in October 2014, it steadily replaced the previous circulating GII.4 Sydney2012 strain, which was the dominant circulating genotype for the past 2 years. As norovirus are the important cause of nonbacterial gastroenteritis, continuous and comprehensive study of the norovirus strains involved in large and cost-effective acute gastroenteritis would help understanding the molecular epidemiology of norovirus infections and development of improved prevention and control measures.
| S-EPMC4566299 | biostudies-literature
Project description:BackgroundNoroviruses (NoVs) are the most common cause of non-bacterial acute gastroenteritis (AGE) in all age groups worldwide. The NoVs circulating in Huzhou over the past 7 years were predominantly GII.4 genotypes. In the winter of 2014-2015, a novel variant of NoV GII.17 emerged and became predominant. We report the epidemiological patterns and genetic characteristics of NoV after the appearance of GII.17 in Huzhou City, Zhejiang, China.MethodsBetween January and December 2015, 746 stool specimens collected from patients with acute gastroenteritis were screened for NoV. Real-time RT-PCR (qPCR) was performed for NoV detection. RT-PCR was used for genomic amplification and sequencing. Genogroups and genotypes were assigned using an online NoV typing tool ( http://www.rivm.nl/mpf/norovirus/typingtool ). Phylogenetic analyses were conducted using MEGA (ver. 6.06).ResultsIn total, 196 (26.3%) specimens were identified as NoV-positive. NoV infection was found in all age groups tested (≤5, 6-15, 16-40, 41-60, and ≥60 years), with the 16-40-year age group having the highest detection rate (117/196, 59.7%). Of the 196 NoV-positive specimens, 191 (97.5%) viruses belonged to GII, and 4 (2.0%) to GI; one sample showed GI and GII co-infection. Overall, 117 (59.7%) viruses were sequenced, and new GII.P17/GII.17 variants were the dominant genotype, accounting for 75.2%, followed by GII.Pe/GII.4 Sydney 2012 strains (11.11%). AGE patients infected with the GII.P17/GII.17 genotypes almost all had abdominal pain and watery stools.ConclusionsWe report the epidemiological patterns and genetic characteristics of the emergence GII.17 over the GII.4 in Huzhou between January and December 2015. After the emergence of GII.17 in October 2014, it steadily replaced the previously circulating GII.4 Sydney 2012 strain, and continued to be dominant in 2015.
| S-EPMC5126990 | biostudies-literature
Project description:BackgroundIn late 2016, an uncommon recombinant NoV genotype called GII.P16-GII.2 caused a sharp increase in outbreaks of acute gastroenteritis in different countries of Asia and Europe, including China. However, we did not observe a drastic increase in sporadic norovirus cases in the winter of 2016 in Huzhou. Therefore, we investigate the prevalence and genetic diversity of NoVs in the sporadic acute gastroenteritis (AGE) cases from January 2016 to December 2017 in Huzhou City, Zhejiang, China.MethodsFrom January 2016 to December 2017, a total of 1001 specimens collected from patients with AGE were screened for NoV by real-time RT-PCR. Partial sequences of the RNA-dependent RNA polymerase (RdRp) and capsid gene of the positive samples were amplified by RT-PCR and sequenced. Genotypes of NoV were confirmed by online NoV typing tool and phylogenetic analysis. Complete VP1 sequences of GII.P16-GII.2 strains detected in this study were further obtained and subjected into sequence analysis.ResultsIn total, 204 (20.4%) specimens were identified as NoV-positive. GII genogroup accounted for most of the NoV-infected cases (98.0%, 200/204). NoV infection was found in all age groups tested (< 5, 5-15, 16-20, 21-30, 31-40, 41-50, 51-60, and >60 years), with the 5-15 year age group having the highest detection rate (17/49, 34.7%). Higher activity of NoV infection could be seen in winter-spring season. The predominant NoV genotypes have changed from GII.Pe-GII.4 Sydney2012 and GII.P17-GII.17 in 2016 to GII.P16-GII.2, GII.Pe-GII.4 Sydney2012 and GII.P17-GII.17 in 2017. Phylogenetic analyses revealed that 2016-2017 GII.P16-GII.2 strains were most closely related to Japan 2010-2012 cluster in VP1 region and no common mutations were found in the amino acids of the HBGA-binding sites and the predicted epitopes.ConclusionsWe report the emergence of GII.P16-GII.2 strains and characterize the molecular epidemiological patterns NoV infection between January 2016 and December 2017 in Huzhou. The predominant genotypes of NoV during our study period are diverse. VP1 amino acid sequences of 2016-2017 GII.P16-GII.2 strains remain static after one year of circulation.
| S-EPMC6056945 | biostudies-literature
Project description:Since 2014, novel non-GII.4 norovirus (NoV) genotypes continue to be reported as the main cause of outbreaks worldwide. In this study, we analyzed the epidemiological and genetic features of NoV outbreaks from July 2014 to June 2018 in Huzhou, China. A total of 450 stool samples collected from 51 AGE outbreaks were tested for NoVs by real-time RT PCR. Partial polymerase and capsid sequences of NoV-positive samples were amplified and sequenced for phylogenetic analysis. NoVs were found to be responsible of 84.3% of AGE outbreaks in Huzhou over the past 5 years. Most NoV outbreaks were reported in the cool months (November-March) and occurred in primary schools and kindergartens. Changes in the diversity of genotypes and the distribution of predominant types were observed in recent years. At least eight genotypes were identified, and 91.9% of the genotyped outbreaks were caused by non-GII.4 strains. The top three circulating genotypes during the study period were GII.2[P16], GII.3[P12], and GII.17[P17]. The predominant NoV genotypes in outbreaks have changed from GII.4 variants to GII.17[P17] in 2014-2015, GII.3[P12] in 2015-2016, and then GII.2[P16] in 2016-2018. Non-GII.4 NoVs play an increasingly important role in outbreaks in Huzhou. Continuous surveillance is needed to monitor the emergence of novel NoV strains and help control NoV outbreaks in the next epidemic season.
| S-EPMC7222896 | biostudies-literature
Project description:Noroviruses (NoVs) cause epidemic acute gastroenteritis, in which histo-blood group antigens (HBGAs) may play an important role in the host susceptibility. To further explore this issue, two outbreaks of acute gastroenteritis caused by a GII.4 and a GII.3 NoV, respectively, in China in 2009 were studied. Stool and saliva samples from symptomatic patients and water samples from the outbreak facilities were collected. RT-PCR showed that 23 out of 33 (GII.4 outbreak) and 12 out of 13 (GII.3outbreak) stool samples were NoV positive. For the GII.4 outbreak the NoV sequences of stool and water samples were from an identical GII.4 strain, while the same GII.3 NoV sequences were found in five stool samples from the GII.3 outbreak. The HBGA phenotypes (A, B, Le(a), Le(b), Le(x), and Le(y)) of all saliva samples were determined, which revealed both secretors and nonsecretors in the symptomatic groups of the two outbreaks. In the GII.3 outbreak, type O individuals appeared less susceptible, while the type A may be more at risk of infection. However, No preference of HBGAs was observed in the GII.4 outbreak. The observation that nonsecretors were infected in both outbreaks differed from the previous results that nonsecretors are resistant to these two GII NoVs.
| S-EPMC3589376 | biostudies-literature
Project description: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.
| S-EPMC5102426 | biostudies-literature
Project description:Over the last fifteen years there have been five pandemics of norovirus (NoV) associated gastroenteritis, and the period of stasis between each pandemic has been progressively shortening. NoV is classified into five genogroups, which can be further classified into 25 or more different human NoV genotypes; however, only one, genogroup II genotype 4 (GII.4), is associated with pandemics. Hence, GII.4 viruses have both a higher frequency in the host population and greater epidemiological fitness. The aim of this study was to investigate if the accuracy and rate of replication are contributing to the increased epidemiological fitness of the GII.4 strains. The replication and mutation rates were determined using in vitro RNA dependent RNA polymerase (RdRp) assays, and rates of evolution were determined by bioinformatics. GII.4 strains were compared to the second most reported genotype, recombinant GII.b/GII.3, the rarely detected GII.3 and GII.7 and as a control, hepatitis C virus (HCV). The predominant GII.4 strains had a higher mutation rate and rate of evolution compared to the less frequently detected GII.b, GII.3 and GII.7 strains. Furthermore, the GII.4 lineage had on average a 1.7-fold higher rate of evolution within the capsid sequence and a greater number of non-synonymous changes compared to other NoVs, supporting the theory that it is undergoing antigenic drift at a faster rate. Interestingly, the non-synonymous mutations for all three NoV genotypes were localised to common structural residues in the capsid, indicating that these sites are likely to be under immune selection. This study supports the hypothesis that the ability of the virus to generate genetic diversity is vital for viral fitness.
| S-EPMC2847951 | biostudies-literature
Project description:An early increase in outbreaks of norovirus gastroenteritis characterised at the French National Reference Centre occurred this winter season. They were concurrent with an unusual pattern of circulating strains, with three predominant genotypes: the re-emergent variant GII.P4 2009-GII.4 2012 found in 28% of norovirus outbreaks and two new emergent recombinant strains GII.P16-GII.4 2012 and GII.P16-GII.2 never before observed in France, found in 24% and 14% of norovirus outbreaks, respectively.
| S-EPMC5476982 | biostudies-literature
Project description:The predominance and continual emergence of new variants in GII-4 noroviruses (NVs) in recent years have raised questions about the role of host immunity and histo-blood group antigens (HBGAs) in NV evolution. To address these questions, we performed a genetic and phenotypic characterization of GII-4 variants circulating in the past decade (1998 to 2008). Ninety-three GII-4 sequences were analyzed, and of them, 16 strains representing 6 genetic clusters were selected for further characterization. The HBGA binding properties were determined by both saliva- and oligosaccharide-binding assays using P particles as a model of NV capsid. The antigenic properties were also examined by enzyme immunoassay (EIA), Western blot analysis, and receptor blocking assay, using P-particle-specific antibodies from immunized mice and GII-4 virus-infected patients. Our results showed that 15 of the 16 GII-4 viruses bound to saliva of all A, B, and O secretors. Oligosaccharide binding assays yielded largely consistent results, although the binding affinities to some oligosaccharides varied among some strains. The only nonbinder had a mutation in the binding site. While antigenic variations were detected among the 16 strains, significant cross-blocking on the HBGA binding was also noted. Sequence alignment revealed high conservation of HBGA binding interfaces with some variations in adjacent regions. Taken together, our data suggested that the ability of GII-4 to recognize different secretor HBGAs persisted over the past decade, which may explain the predominance of GII-4 over other genotypes. Our data also indicated that both the host immunity and HBGAs play a role in NV evolution. While host immunity may continue driving NV for antigenic change, the functional selection by the HBGAs tends to lock the architecture of the capsid/HBGA interfaces and allows only limited variations outside the HBGA binding sites. A potential outcome of such counterselection between theses two factors in NV evolution is discussed.
| S-EPMC2937647 | biostudies-literature
Project description:The control of re-occurring pandemic pathogens requires understanding the origins of new pandemic variants and the factors that drive their global spread. This is especially important for GII.4 norovirus, where vaccines under development offer promise to prevent hundreds of millions of annual gastroenteritis cases. Previous studies have hypothesized that new GII.4 pandemic viruses arise when previously circulating pandemic or pre-pandemic variants undergo substitutions in antigenic regions that enable evasion of host population immunity, as described by conventional models of antigenic drift. In contrast, we show here that the acquisition of new genetic and antigenic characteristics cannot be the proximal driver of new pandemics. Pandemic GII.4 viruses diversify and spread over wide geographical areas over several years prior to simultaneous pandemic emergence of multiple lineages, indicating that the necessary sequence changes must have occurred before diversification, years prior to pandemic emergence. We confirm this result through serological assays of reconstructed ancestral virus capsids, demonstrating that by 2003, the ancestral 2012 pandemic strain had already acquired the antigenic characteristics that allowed it to evade prevailing population immunity against the previous 2009 pandemic variant. These results provide strong evidence that viral genetic changes are necessary but not sufficient for GII.4 pandemic spread. Instead, we suggest that it is changes in host population immunity that enable pandemic spread of an antigenically preadapted GII.4 variant. These results indicate that predicting future GII.4 pandemic variants will require surveillance of currently unsampled reservoir populations. Furthermore, a broadly acting GII.4 vaccine will be critical to prevent future pandemics.
| S-EPMC7751145 | biostudies-literature