Molecular Evolution of the RNA-Dependent RNA Polymerase and Capsid Genes of Human Norovirus Genotype GII.2 in Japan during 2004–2015

Mizukoshi, Fuminori; Nagasawa, Kinzo; Doan, Yen Hai; Haga, Kei; Yoshizumi, Shima; Ueki, Yo; Shinohara, Michiyo; Ishikawa, Mariko; Sakon, Naomi; Shigemoto, Norifumi; Okamoto-Nakagawa, Reiko; Ochi, Akihiro; Murakami, Koichi; Ryo, Akihide; Suzuki, Yoshiyuki; Katayama, Kazuhiko; Kimura, Hirokazu

doi:10.3389/fmicb.2017.00705

Cited by 21 publications

(30 citation statements)

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“…We found that the rate of the HuNoV VP1 gene in GII.2 strains, including 2016 strains was 3.26 × 10 -3 substitutions/site/year. However, previous studies showed different evolutionary rates ( Eden et al, 2014 ; Kobayashi et al, 2016 ; Mizukoshi et al, 2017 ). For example, Kobayashi et al (2016) suggested it was around 3.76 × 10 -3 substitutions/site/year for the VP1 gene of all HuNoV GII.…”

Section: Discussionmentioning

confidence: 90%

“…Our main findings are as follows. (1) A common ancestor of the VP1 gene of the 2016 strains diverged from another GII.P16-GII.2 strain around 10 years ago with an evolutionary rate as described ( Mizukoshi et al, 2017 ) ( Figure 1 ). (2) A common ancestor of the RdRp region of the 2016 strains diverged from the RdRp region of the GII.P16-GII.4 rather than the previous GII.P16-GII.2 strains in 1999 with a rapid evolutionary rate (around 10 -3 substitutions/site/year) ( Figure 2 ).…”

Section: Discussionmentioning

confidence: 99%

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Genetic Analysis of Human Norovirus Strains in Japan in 2016–2017

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In the 2016/2017 winter season in Japan, HuNoV GII.P16-GII.2 strains (2016 strains) emerged and caused large outbreaks of acute gastroenteritis. To better understand the outbreaks, we examined the molecular evolution of the VP1 gene and RdRp region in 2016 strains from patients by studying their time-scale evolutionary phylogeny, positive/negative selection, conformational epitopes, and phylodynamics. The time-scale phylogeny suggested that the common ancestors of the 2016 strains VP1 gene and RdRp region diverged in 2006 and 1999, respectively, and that the 2016 strain was the progeny of a pre-2016 GII.2. The evolutionary rates of the VP1 gene and RdRp region were around 10-3 substitutions/site/year. Amino acid substitutions (position 341) in an epitope in the P2 domain of 2016 strains were not found in pre-2016 GII.2 strains. Bayesian skyline plot analyses showed that the effective population size of the VP1 gene in GII.2 strains was almost constant for those 50 years, although the number of patients with NoV GII.2 increased in 2016. The 2016 strain may be involved in future outbreaks in Japan and elsewhere.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Genetic Analysis of Human Norovirus Strains in Japan in 2016–2017

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“…Next, we estimated the HuNoV GII.4 VP1 gene evolutionary rate as 7.68 × 10 −3 substitutions/site/year. Our observations are generally consistent with previous observations overall, with GII.4 having a higher evolutionary rate than other genotypes such as GII.7 (2.3 × 10 −3 substitutions/site/year), GII.3 (4.16 × 10 −3 substitutions/site/year), and GII.2 (1.31 × 10 −3 substitutions/site/year) (Bok et al, 2009 ; Bull et al, 2010 ; Siebenga et al, 2010 ; Boon et al, 2011 ; Fioretti et al, 2014 ; Qiao et al, 2016 ; Mizukoshi et al, 2017 ; Parra et al, 2017 ). In addition, we estimated the different evolutionary rates among GII.4 variants.…”

Section: Discussionmentioning

confidence: 99%

“…The values obtained by dividing the numbers of chain lengths by that of the log parameters were used as sample sizes. For the phylogenetic distance analyses, we acquired 3–11,440 data that exhibited the number of all combinations between GII.4 strains included in the dataset (Mizukoshi et al, 2017 ). Detailed statistical data are shown in Tables S2 – S4 .…”

Section: Methodsmentioning

confidence: 99%

Molecular Evolution of the VP1 Gene in Human Norovirus GII.4 Variants in 1974–2015

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Human norovirus (HuNoV) is a leading cause of viral gastroenteritis worldwide, of which GII.4 is the most predominant genotype. Unlike other genotypes, GII.4 has created various variants that escaped from previously acquired immunity of the host and caused repeated epidemics. However, the molecular evolutionary differences among all GII.4 variants, including recently discovered strains, have not been elucidated. Thus, we conducted a series of bioinformatic analyses using numerous, globally collected, full-length GII.4 major capsid (VP1) gene sequences (466 strains) to compare the evolutionary patterns among GII.4 variants. The time-scaled phylogenetic tree constructed using the Bayesian Markov chain Monte Carlo (MCMC) method showed that the common ancestor of the GII.4 VP1 gene diverged from GII.20 in 1840. The GII.4 genotype emerged in 1932, and then formed seven clusters including 14 known variants after 1980. The evolutionary rate of GII.4 strains was estimated to be 7.68 × 10−3 substitutions/site/year. The evolutionary rates probably differed among variants as well as domains [protruding 1 (P1), shell, and P2 domains]. The Osaka 2007 variant strains probably contained more nucleotide substitutions than any other variant. Few conformational epitopes were located in the shell and P1 domains, although most were contained in the P2 domain, which, as previously established, is associated with attachment to host factors and antigenicity. We found that positive selection sites for the whole GII.4 genotype existed in the shell and P1 domains, while Den Haag 2006b, New Orleans 2009, and Sydney 2012 variants were under positive selection in the P2 domain. Amino acid substitutions overlapped with putative epitopes or were located around the epitopes in the P2 domain. The effective population sizes of the present strains increased stepwise for Den Haag 2006b, New Orleans 2009, and Sydney 2012 variants. These results suggest that HuNoV GII.4 rapidly evolved in a few decades, created various variants, and altered its evolutionary rate and antigenicity.

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“…In our study, GII.P16 was detected with the GII.3 capsid genotype circulating in 2015; however, it was grouped in a different cluster than our GII.P16-GII.4 Sydney strains and previous strains detected in AGE outbreaks in Southern Brazil between 2010 and 2011 [ 10 ]. Recently, GII.P16 re-emerged combined with GII.2 grouped in the same cluster as the polymerase GII.P16 of the new recombinant GII.P16-GII.4 Sydney, differing from the previous one and suggesting the importance of the current GII.P16 polymerase in norovirus circulation worldwide [ 18 , 19 , 47 , 48 , 49 , 50 , 51 , 52 ]. The authors also described the importance of the polymerase for viral fitness and variability [ 19 ]; therefore, the newly acquired polymerase could play a role in the success of this recombinant form.…”

Section: Discussionmentioning

confidence: 99%

Detection and molecular characterization of the novel recombinant norovirus GII.P16-GII.4 Sydney in southeastern Brazil in 2016

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Noroviruses are the leading cause of acute gastroenteritis (AGE) in all age groups worldwide. Despite the high genetic diversity of noroviruses, most AGE outbreaks are caused by a single norovirus genotype: GII.4. Since 1995, several different variants of norovirus GII.4 have been associated with pandemics, with each variant circulating for 3 to 8 years. The Sydney_2012 variant was first reported in Australia and then in other countries. A new variant, GII.P16-GII.4, was recently described in Japan and South Korea and then in the USA, France, Germany and England. In our study, 190 faecal specimens were collected from children admitted to a paediatric hospital and a public health facility during a surveillance study of sporadic cases of AGE conducted between January 2015 and July 2016. The norovirus was detected by RT-qPCR in 51 samples (26.8%), and in 37 of them (72.5%), the ORF1-2 junction was successfully sequenced. The new recombinant GII.P16-GII.4 Sydney was revealed for the first time in Brazil in 2016 and predominated among other strains (9 GII.Pe-GII.4, 3 GII.P17-GII.17, 1 GII.Pg-GII.1, 1 GII.P16-GII.3 and 1 GII.PNA-GII.4). The epidemiological significance of this new recombinant is still unknown, but continuous surveillance studies may evaluate its impact on the population, its potential to replace the first recombinant GII.Pe-GII.4 Sydney 2012 variant, and the emergence of new recombinant forms of GII.P16.

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Molecular Evolution of the RNA-Dependent RNA Polymerase and Capsid Genes of Human Norovirus Genotype GII.2 in Japan during 2004–2015

Cited by 21 publications

References 8 publications

Genetic Analysis of Human Norovirus Strains in Japan in 2016–2017

Genetic Analysis of Human Norovirus Strains in Japan in 2016–2017

Molecular Evolution of the VP1 Gene in Human Norovirus GII.4 Variants in 1974–2015

Detection and molecular characterization of the novel recombinant norovirus GII.P16-GII.4 Sydney in southeastern Brazil in 2016

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