scholarly journals Norovirus GII.2[P16] strain in Shenzhen, China: a retrospective study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Wang ◽  
Miao Jin ◽  
Hailong Zhang ◽  
Yanan Zhu ◽  
Hong Yang ◽  
...  

Abstract Background Norovirus (NoV) is the main cause of non-bacterial acute gastroenteritis (AGE) outbreaks worldwide. From September 2015 through August 2018, 203 NoV outbreaks involving 2500 cases were reported to the Shenzhen Center for Disease Control and Prevention. Methods Faecal specimens for 203 outbreaks were collected and epidemiological data were obtained through the AGE outbreak surveillance system in Shenzhen. Genotypes were determined by sequencing analysis. To gain a better understanding of the evolutionary characteristics of NoV in Shenzhen, molecular evolution and mutations were evaluated based on time-scale evolutionary phylogeny and amino acid mutations. Results A total of nine districts reported NoV outbreaks and the reported NoV outbreaks peaked from November to March. Among the 203 NoV outbreaks, 150 were sequenced successfully. Most of these outbreaks were associated with the NoV GII.2[P16] strain (45.3%, 92/203) and occurred in school settings (91.6%, 186/203). The evolutionary rates of the RdRp region and the VP1 sequence were 2.1 × 10–3 (95% HPD interval, 1.7 × 10–3–2.5 × 10–3) substitutions/site/year and 2.7 × 10–3 (95% HPD interval, 2.4 × 10–3–3.1 × 10–3) substitutions/site/year, respectively. The common ancestors of the GII.2[P16] strain from Shenzhen and GII.4 Sydney 2012[P16] diverged from 2011 to 2012. The common ancestors of the GII.2[P16] strain from Shenzhen and previous GII.2[P16] (2010–2012) diverged from 2003 to 2004. The results of amino acid mutations showed 6 amino acid substitutions (*77E, R750K, P845Q, H1310Y, K1546Q, T1549A) were found only in GII.4 Sydney 2012[P16] and the GII.2[P16] recombinant strain. Conclusions This study illustrates the molecular epidemiological patterns in Shenzhen, China, from September 2015 to August 2018 and provides evidence that the epidemic trend of GII.2[P16] recombinant strain had weakened and the non-structural proteins of the recombinant strain might have played a more significant role than VP1.

2020 ◽  
Author(s):  
Jing Wang ◽  
Miao Jin ◽  
Hailong Zhang ◽  
Yanan Zhu ◽  
Hong Yang ◽  
...  

Abstract Background: Norovirus (NoV) is the main cause of non-bacterial acute gastroenteritis (AGE) outbreaks worldwide. From September 2015 through August 2018, 203 NoV outbreaks involving 2,500 cases were reported to the Shenzhen Center for Disease Control and Prevention.Methods: Faecal specimens for 203 outbreaks were collected and epidemiological data were obtained through the AGE outbreak surveillance system in Shenzhen. Genotypes were determined by sequencing analysis. To gain a better understanding of the evolutionary characteristics of NoV in Shenzhen, recombination events were analysed and molecular evolution was evaluated based on time-scale evolutionary phylogeny and amino acid mutations.Results: A total of nine counties reported NoV outbreaks and the reported NoV outbreaks peaked from November to March. Among the 203 NoV outbreaks, 150 were sequenced successfully. Most of these outbreaks were associated with the NoV GII.2[P16] strain (45.3%, 92/203) and occurred in school settings (91.6%, 186/203). The GII.2[P16] strain is a recombinant strain that is relatively stable. In these GII.2[P16] recombination strain outbreaks, the non-structural proteins of the recombination strain might have played a more significant role than VP1.Conclusions: This study illustrates the molecular epidemiological patterns in Shenzhen, China, from September 2015 to August 2018 and provides evidence that the GII.2[P16] strain was relatively stable and that epidemic trend has weakened.


2020 ◽  
Author(s):  
Jing Wang ◽  
Miao Jin ◽  
Hailong Zhang ◽  
Yanan Zhu ◽  
Hong Yang ◽  
...  

Abstract Background Norovirus (NoV) is the main cause of non-bacterial acute gastroenteritis (AGE) outbreaks worldwide. From September 2015 through August 2018, 203 NoV outbreaks with 2,500 patients were reported to the Shenzhen Center for Disease Control and Prevention. Methods Fecal specimens were collected from the 203 outbreaks and epidemiological data were collected through the AGE outbreak surveillance system in Shenzhen. The genotypes were determined by sequencing analysis. To gain a better understanding of evolutionary characterization of NoV in Shenzhen, the molecular evolution was analyzed by time-scale evolutionary phylogeny and amino acid mutations. Results Most of these outbreaks were associated with NoV GII.P16/GII.2 strain (45.3%,92/203) and occurred in school settings (91.6%,186/203). The timescale phylogeny suggested that the GII.P16/GII.2 strain was recombination strain and were still stable. The amino acid mutations suggested that the nonstructural proteins of the recombination strain might play a more significant role than VP1 gene in these GII.P16/GII.2 recombination strain outbreaks. Conclusions This study illustrated the characteristics of the molecular epidemiological patterns in Shenzhen, China during September 2015 to August 2018 and provided the evidence that the GII.P16/GII.2 strain was static and the epidemic trend had fade.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Gunadi ◽  
Hendra Wibawa ◽  
Mohamad Saifudin Hakim ◽  
Marcellus ◽  
Ika Trisnawati ◽  
...  

Abstract Background Transmission within families and multiple spike protein mutations have been associated with the rapid transmission of SARS-CoV-2. We aimed to: (1) describe full genome characterization of SARS-CoV-2 and correlate the sequences with epidemiological data within family clusters, and (2) conduct phylogenetic analysis of all samples from Yogyakarta and Central Java, Indonesia and other countries. Methods The study involved 17 patients with COVID-19, including two family clusters. We determined the full-genome sequences of SARS-CoV-2 using the Illumina MiSeq next-generation sequencer. Phylogenetic analysis was performed using a dataset of 142 full-genomes of SARS-CoV-2 from different regions. Results Ninety-four SNPs were detected throughout the open reading frame (ORF) of SARS-CoV-2 samples with 58% (54/94) of the nucleic acid changes resulting in amino acid mutations. About 94% (16/17) of the virus samples showed D614G on spike protein and 56% of these (9/16) showed other various amino acid mutations on this protein, including L5F, V83L, V213A, W258R, Q677H, and N811I. The virus samples from family cluster-1 (n = 3) belong to the same clade GH, in which two were collected from deceased patients, and the other from the survived patient. All samples from this family cluster revealed a combination of spike protein mutations of D614G and V213A. Virus samples from family cluster-2 (n = 3) also belonged to the clade GH and showed other spike protein mutations of L5F alongside the D614G mutation. Conclusions Our study is the first comprehensive report associating the full-genome sequences of SARS-CoV-2 with the epidemiological data within family clusters. Phylogenetic analysis revealed that the three viruses from family cluster-1 formed a monophyletic group, whereas viruses from family cluster-2 formed a polyphyletic group indicating there is the possibility of different sources of infection. This study highlights how the same spike protein mutations among members of the same family might show different disease outcomes.


2017 ◽  
Author(s):  
Trevor Bedford ◽  
Richard A. Neher

AbstractThis report details current seasonal influenza circulation patterns as of Sep 2017 and makes projections up to Sep 2018 to coincide with selection of the 2018 Southern Hemisphere vaccine strain. This is not meant as a comprehensive report, but is instead intended as particular observations that we’ve made that may be of relevance. Please also note that observed patterns reflect the GISAID database and may not be entirely representative of underlying dynamics. All analyses are based on the nextflu pipeline [1] with continual updates posted to nextflu.org.A/H3N2H3N2 continues to diversify with many coexisting clades, all of which carry several amino acid mutations at previously characterized epitope sites. The majority of viruses fall into the 3c2.a clade which has been dominating globally for >3 years, but 3c3.a viruses continue to persist. The common ancestor of circulating H3N2 viruses is now more than 5 years old, which is rare for H3N2. Despite extensive genetic diversity, serological assays suggest limited, but non-zero, antigenic evolution. We expect multiple competing clades within 3c2.a to persist into the future with no clear immediate winner.A/H1N1pdmA clade comprising mutations S74R and I295V has recently risen to >60% global frequency. Although it shows no antigenic distinction by ferret HI data, the rapidity of its rise suggests a selective origin.B/VicA clade with a two amino acid deletion 162-/163-has altered serological properties and is increasing in frequency, albeit slowly. Two other clades (carrying mutations K209N and V87A/I175V) have increased in frequency moderately.B/YamA clade comprising M251V within clade 3 viruses continues to dominate. The is little genetic differentiation within this clade and no evidence of antigenic evolution.


2021 ◽  
pp. 1-13
Author(s):  
Salvatore Dimonte ◽  
Muhammed Babakir-Mina ◽  
Taib Hama-Soor ◽  
Salar Ali

<b><i>Introduction:</i></b> SARS-CoV-2 is a new type of coronavirus causing a pandemic severe acute respiratory syndrome (SARS-2). Coronaviruses are very diverting genetically and mutate so often periodically. The natural selection of viral mutations may cause host infection selectivity and infectivity. <b><i>Methods:</i></b> This study was aimed to indicate the diversity between human and animal coronaviruses through finding the rate of mutation in each of the spike, nucleocapsid, envelope, and membrane proteins. <b><i>Results:</i></b> The mutation rate is abundant in all 4 structural proteins. The most number of statistically significant amino acid mutations were found in spike receptor-binding domain (RBD) which may be because it is responsible for a corresponding receptor binding in a broad range of hosts and host selectivity to infect. Among 17 previously known amino acids which are important for binding of spike to angiotensin-converting enzyme 2 (ACE2) receptor, all of them are conservative among human coronaviruses, but only 3 of them significantly are mutated in animal coronaviruses. A single amino acid aspartate-454, that causes dissociation of the RBD of the spike and ACE2, and F486 which gives the strength of binding with ACE2 remain intact in all coronaviruses. <b><i>Discussion/Conclusion:</i></b> Observations of this study provided evidence of the genetic diversity and rapid evolution of SARS-CoV-2 as well as other human and animal coronaviruses.


2012 ◽  
Vol 57 (1) ◽  
pp. 436-444 ◽  
Author(s):  
Naoki Ogura ◽  
Yukiyo Toyonaga ◽  
Izuru Ando ◽  
Kunihiro Hirahara ◽  
Tsutomu Shibata ◽  
...  

ABSTRACTJTK-853, a palm site-binding NS5B nonnucleoside polymerase inhibitor, shows antiviral activityin vitroand in hepatitis C virus (HCV)-infected patients. Here, we report the results of genotypic and phenotypic analyses of resistant variants in 24 HCV genotype 1-infected patients who received JTK-853 (800, 1,200, or 1,600 mg twice daily or 1,200 mg three times daily) in a 3-day monotherapy. Viral resistance in NS5B was investigated using HCV RNA isolated from serum specimens from the patients. At the end of treatment (EOT) with JTK-853, the amino acid substitutions M414T (methionine [M] in position 414 at baseline was replaced with threonine [T] at EOT), C445R (cysteine [C] in position 445 at baseline was replaced with arginine [R] at EOT), Y448C/H (tyrosine [Y] in position 448 at baseline was replaced with cysteine [C] or histidine [H] at EOT), and L466F (leucine [L] in position 466 at baseline was replaced with phenylalanine [F] at EOT), which are known to be typical resistant variants of nonnucleoside polymerase inhibitors, were observed in a clonal sequencing analysis. These substitutions were also selected by a treatment with JTK-853in vitro, and the 50% effective concentration of JTK-853 in the M414T-, C445F-, Y448H-, and L466V-harboring replicons attenuated the susceptibility by 44-, 5-, 6-, and 21-fold, respectively, compared with that in the wild-type replicon (Con1). These findings suggest that amino acid substitutions of M414T, C445R, Y448C/H, and L466F are thought to be viral resistance mutations in HCV-infected patients receiving JTK-853 in a 3-day monotherapy.


1986 ◽  
Vol 7 (5) ◽  
pp. 213-216 ◽  
Author(s):  
Gianfranco Cossu ◽  
Mario Manca ◽  
Pier Giorgio Righetti ◽  
Elisabetta Gianazza ◽  
VÉRonique Baudin ◽  
...  

2006 ◽  
Vol 27 (9) ◽  
pp. 926-937 ◽  
Author(s):  
Yum L. Yip ◽  
Vincent Zoete ◽  
Holger Scheib ◽  
Olivier Michielin

2000 ◽  
Vol 18 (2) ◽  
pp. 126-134 ◽  
Author(s):  
Nicky K.C Wong ◽  
David V Renouf ◽  
Sylvain Lehmann ◽  
Elizabeth F Hounsell

Author(s):  
Paul L. Boyer ◽  
Catherine A. Rehm ◽  
Michael C. Sneller ◽  
JoAnn Mican ◽  
Margaret R. Caplan ◽  
...  

Resistance to anti-Human Immunodeficiency Virus (HIV) drugs has been a problem from the beginning of antiviral drug treatments. The recent expansion of combination antiretroviral therapy worldwide has led to an increase in resistance to antiretrovirals; understanding the mechanisms of resistance is increasingly important. In this study, we analyzed reverse transcriptase (RT) variants based on sequences derived from an individual who had a low-level rebound viremia while undergoing therapy with abacavir, azidothymidine (AZT or Zidovudine), and (−)-L-2′,3′-dideoxy-3′-thiacytidine (Lamivudine or 3TC). The RT had mutations at positions 64, 67, 70, 184, 219, and a threonine insertion after amino acid 69 in RT. The virus remained partially susceptible to the nucleoside reverse transcriptase inhibitor (NRTI) regimen. We show how these mutations affect the ability of NRTIs to inhibit DNA synthesis by RT. The presence of the inserted threonine reduced the susceptibility of the RT mutant to inhibition by Tenofovir.


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