Echovirus plays major roles in the natural recombination of Coxsackievirus B3

Shen, Han‐Xi; Liu, Tingjun; Yu-cheng, Luo; Shao, Shihe; Deng, Xintao; Wang, Hua

doi:10.1002/jmv.24929

Cited by 7 publications

(3 citation statements)

References 27 publications

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“…We allocated the worldwide CVB3 variants to twenty-three different evolutionary recombinant lineages based on non-capsid sequences. Several previous studies showed that Chinese CVB3 showed the highest similarity with the parental CVB3 in the P1 region, with the E25 strain in the P2-P3 region, and other strains of CVB3 showed similarity with CVB5 in the P3 region [ 54 , 55 ], which is consistent with our study. However, it remains unclear whether there are substantial differences in recombination frequencies between different EVs such as echoviruses, and whether CVB5 plays a major role in the natural recombination of CVB3.…”

Section: Discussionsupporting

confidence: 92%

Whole-genome analysis of coxsackievirus B3 reflects its genetic diversity in China and worldwide

Yang

Yan

Song

et al. 2022

Virol J

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Background Coxsackievirus B3 (CVB3) has emerged as an active pathogen in myocarditis, aseptic meningitis, hand, foot, and mouth disease (HFMD), and pancreatitis, and is a heavy burden on public health. However, CVB3 has not been systematically analyzed with regard to whole-genome diversity and recombination. Therefore, this study was undertaken to systematically examine the genetic characteristics of CVB3 based on its whole genome. Methods We combined CVB3 isolates from our national HFMD surveillance and global sequences retrieved from GenBank. Phylogenetic analysis was performed to examine the whole genome variety and recombination forms of CVB3 in China and worldwide. Results Phylogenetic analysis showed that CVB3 strains isolated worldwide could be classified into clusters A–E based on the sequence of the entire VP1 region. The predominant CVB3 strains in China belonged to cluster D, whereas cluster E CVB3 might be circulated globally compared to other clusters. The average nucleotide substitution rate in the P1 region of CVB3 was 4.82 × 10–3 substitutions/site/year. Myocarditis was more common with cluster A. Clusters C and D presented more cases of acute flaccid paralysis, and cluster D may be more likely to cause HFMD. Multiple recombination events were detected among CVB3 variants, and there were twenty-three recombinant lineages of CVB3 circulating worldwide. Conclusions Overall, this study provides full-length genomic sequences of CVB3 isolates with a wide geographic distribution over a long-term time scale in China, which will be helpful for understanding the evolution of this pathogen. Simultaneously, continuous surveillance of CVB3 is indispensable to determine its genetic diversity in China as well as worldwide.

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Section: Discussionsupporting

confidence: 92%

Whole-genome analysis of coxsackievirus B3 reflects its genetic diversity in China and worldwide

Yang

Yan

Song

et al. 2022

Virol J

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“…The emergence of E30 has been found to exhibit a cyclic pattern with dominance and disappearance of individual recombinants over a period of years [21][22][23][24][25][26][27]. The turnover period for such recombinants has been calculated to be from 1.8 to 5 years [28,29].…”

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confidence: 99%

Genetic characterization of a novel recombinant echovirus 30 strain causing a regional epidemic of aseptic meningitis in Hokkaido, Japan, 2017

et al. 2019

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A regional epidemic of aseptic meningitis caused by echovirus 30 (E30) occurred in Hokkaido, Japan, during the period of August-December 2017. To investigate their phylogenetic relationship to other human enteroviruses, we determined the complete genomic nucleotide sequences of isolates from this outbreak. Phylogenetic analysis of the viral capsid protein 1 gene showed that the strains were most closely related to E30 strains detected in Germany, France, and Russia in 2013. In contrast, the region encoding the viral protease and the RNA-dependent RNA polymerase had a close phylogenetic relationship to non-E30 enteroviruses detected in the United Kingdom and Switzerland in 2015-2017, suggesting that a recombination event had occurred.

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“…Various infectious agents contribute to myocarditis, including bacteria, viruses, and parasites to allergens or toxins 4 . Coxsackievirus type B3 (CVB3) is regarded an important cause of viral myocarditis 5 . Achievements in cardiac magnetic resonance imaging and molecular detection of viruses have been made to better understand the mechanisms of viral myocarditis.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐425‐3p inhibits myocardial inflammation and cardiomyocyte apoptosis in mice with viral myocarditis through targeting TGF‐β1

Gao

et al. 2020

Immunity Inflam & Disease

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Objective Emerging articles have profiled the relations between microRNAs and viral myocarditis. This research was unearthed to explore the capacity of miR‐425‐3p on cardiomyocyte apoptosis in mice with viral myocarditis and its mechanism. Methods A total of 120 mice were classified into 4 groups in a random fashion (n = 30). The mice were intraperitoneally injected with coxsackievirus type B3 (CVB3) to induce myocarditis. On the 7th day after CVB3 infection, 10 mice in each group were euthanized to assess the heart function indices of mice, observe the pathological conditions, detect myocardial tissue apoptosis, and measure the inflammatory factor levels in myocardial tissues. Expression of miR‐425‐3p, transforming growth factor (TGF‐β1), and apoptosis‐associated proteins in myocardial tissues was determined. The remaining 20 mice in each group were used for survival observation. The luciferase activity assay was implemented to validate the relationship between miR‐425‐3p and TGF‐β1. miR‐425‐3p mimic was transfected into mouse cardiomyocytes HL‐1 and then infected with CVB3 to further verify the regulatory effect of miR‐425‐3p on the cardiomyocyte apoptosis in viral myocarditis. Results miR‐425‐3p was lowly expressed in myocardial tissues of mice with viral myocarditis. Overexpressed miR‐425‐3p improved the cardiac function, alleviated pathological conditions, reduced cardiomyocyte apoptosis, decreased Bax and cleaved Caspase‐3 expression, elevated Bcl‐2 expression, decreased levels of inflammatory factors and improved survival rate of mice with viral myocarditis. Luciferase activity assay verified that miR‐425‐3p could bind to TGF‐β1, and overexpressed miR‐425‐3p suppressed TGF‐β1, p‐smad2/smad2 and p‐smad3/smad3 expression. In vitro experiments further verified that overexpression of miR‐425‐3p inhibited the apoptosis of CVB3‐HL‐1 cells, and the addition of TGF‐β1 would reverse this effect. Conclusion Our research indicates that miR‐425‐3p is poorly expressed in myocardial tissues of mice with viral myocarditis. Overexpressed miR‐425‐3p inhibits cardiomyocyte apoptosis and myocardial inflammation in mice with viral myocarditis as well as improves their survival rates through suppressing the TGF‐β1/smad axis.

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Echovirus plays major roles in the natural recombination of Coxsackievirus B3

Cited by 7 publications

References 27 publications

Whole-genome analysis of coxsackievirus B3 reflects its genetic diversity in China and worldwide

Whole-genome analysis of coxsackievirus B3 reflects its genetic diversity in China and worldwide

Genetic characterization of a novel recombinant echovirus 30 strain causing a regional epidemic of aseptic meningitis in Hokkaido, Japan, 2017

MicroRNA‐425‐3p inhibits myocardial inflammation and cardiomyocyte apoptosis in mice with viral myocarditis through targeting TGF‐β1

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