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Enterovirus D68 strains worldwide in 2014 and 2016 have caused significant respiratory and neurological problems. In 2018, circulating strains in the B3 and A2 subclades clustered into several subgroups, with different phylogenetic origins. Clusters in subclade B3 emerged from strains circulating in primary and Europe in 2016, but others had deeper roots in Asia's 2016-2016 epidemic, with some clustering to Asian strains, according to clusters in A2, traced back to strains identified in East Asia in 2015-2016. Both 2018 A2 strains in the BC and DE-loops show steady signs of ongoing antigenic evolution, and all 2018 A2 strains have unique patterns in the putative neutralizing epitopes. The pattern in the BC-loop of the USA B3 subgroup's B3 subgroup had not been identified on the continent before. Patients with EV-D68 in subclade A2 were significantly older than those with a B3 subclade virus.
Source link: https://doi.org/10.1371/journal.ppat.1010515
Since the 2014 outbreak, a substantial body of epidemiological evidence has been published on Enterovirus D68 infections. Of the 4,329 articles retrieved from the databases, 89 of the inclusion criteria were from 39 different countries with apparently healthy individuals and patients with acute respiratory infections, acute flaccid myelitis, and asthma-related diseases. Patients with persistent acute respiratory diseases have frequent respiratory problems, according to the CFR estimate, occasional deaths related to EV-D68 infections in patients with severe acute respiratory infections have been reported. According to the present report, sporadic deaths have been linked to advanced respiratory EV-D68 infections. In nearly all participants of the included studies, the report also shows a low incidence of current EV-D68 infections as opposed to the presence of EV-D68 antibodies. These findings have therefore highlighted the need to carry out and/or improve continuous surveillance of EV-D68 infections in hospitals and the community in the hopes of future epidemic response.
Source link: https://doi.org/10.1371/journal.pntd.0010073
Enterovirus D68 was recently identified as an important cause of respiratory disease and acute flaccid myelitis, mostly in children. We examined 472 pediatric patients with acute respiratory disease and screened for EVD68 from April to October 2021. EVD68 was also tested for EVD68 in parallel, samples obtained from a wastewater treatment plant serving the hospitalized patients' residential area were also tested for EVD68. 33 patients were positive for EVD68 RNA from the 472 clinical samples reviewed. This is the first study to use wastewater-based epidemiology to monitor EVD68 variability by quantitative measurement, and it finds a strong correlation with clinically diagnosed cases.
Source link: https://doi.org/10.3390/v14051010
Background: Japan experienced unusual rise in acute asthma hospitalizations of children in September 2015 that coincided with an enterovirus D68 outbreak. The aim of this study was to determine whether EV-D68 had a causal connection with the rise in asthma hospitalizations. Due to acute asthma exacerbation, the Japanese Society of Pediatric Allergy and Clinical Immunology pleaded with its affiliated hospitals to publish monthly counts of hospitalizations, ICU admissions, and mechanical ventilations as a result of acute asthma exacerbation. The Infectious Disease Surveillance Center of Japan had monthly reports of EV-D68 detection. To determine the relationship of EV-D68 detections for asthma exacerbation, a Granger causality test was used. The connection between EV-D68 and asthma hospitalizations/mechanical ventilations was confirmed by a Granger causality study. Conclusions: The rise in pediatric asthma hospitalizations in Japan in September 2015 was found to be connected to the EV-D68 epidemic. Respiratory pathogens can cause asthma exacerbation in u201ce.
Source link: https://doi.org/10.1016/j.alit.2017.04.003
Many studies from different countries have found an increasing number of patients with respiratory disease due to EV-D68 connectivity with relevant clinical severity in recent years. In addition, EV-D68 has been attributed to acute flaccid paralysis and cranial nerve dysfunction in children, raising questions in the community. Protemp diagnosis and continued monitoring of EV-D68 infections are key to preventing new outbreaks and preventing new outbreaks. Moreover, if the connection between EV-D68 and severe illnesses is confirmed, then the adoption of appropriate preventive and therapeutic strategies is a priority.
Source link: https://doi.org/10.3390/v7112925
We discovered that neonatal type I interferon receptor knockout mice are susceptible to EV-D68 infection by intraperitoneal inoculation, and that we were able to recapitulate the paralysis process observed in human disease. Among the EV-D68 strains tested, strain US/MO-14-18949 had no observable disease in this mouse model, but other strains caused paralysis and death. One amino acid change from isoleucine to valine in VP3 attenuated neurovirulence by reducing virus replication in the brain and spinal cord of infected mice.
Source link: https://doi.org/10.3390/v12080867
Although there is no evidence connecting EV-D68 infections and AFM outbreaks in the United States, comprehensive clinical, immunological, and epidemiological evidence points to EV-D68 as the key causative agent of recent seasonal AFM outbreaks. In many ways affecting neurovirulence, including their genetic sequence, receptor activation, the ability to infect neurons, and mouse neuropathogeneticity in mice, this review summarizes findings obtained from in vitro and vitro models of EV-D68-induced disease.
Source link: https://doi.org/10.3390/v11090821
Methods: This prospective cohort study looked at respiratory viral transmission among preschoolers in a public kindergarten in Taipei City, Taiwan, between September 2006 and June 2008. To find specific EV-D68 antibodies and neutralization tests, we performed viral isolation to find acute EV-D68 infection and neutralization tests to detect specific EV-D68 antibodies and seroconversion rates. Among 190 kindergarteners aged from two to five years old, nine children had acute EV-D68 fever in September 2007. Parts of clade A1 The phylogenetic tree of partial viral protein 3 and viral protein 1 was clustered in clade A1. 49 children with initial seronegative and paired sera were 73% on average, according to the seroconversion rate. Conclusions: According to kindergarteners, a high seroconversion rate for EV-D68 was found among kindergarteners, which means that preschool-aged children are highly susceptible to EV-D68 disease and that the disease burden could be highly underestimated.
Source link: https://doi.org/10.1016/j.jmii.2019.04.010
A small number of acute respiratory tract infection cases caused by enterovirus D68 have been reported regularly to Centers for Disease Control and Prevention since 1987 by countries in North America, Europe, and Asia. The National Influenza Centre in Ghana conducts surveillance of respiratory infections, focusing on those caused by influenza virus; however, there are no reports on other viruses that cause respiratory disease in Ghana, including EV-D68. Using a random sampling technique, oropharyngeal and nasopharyngeal swabs from patients with SARI and ILI with human influenza viruses were tested for EV-D68 using real-time reverse transcription chain reaction. Results: Enterovirus D68 was identified in 4 out of 182 SARI samples tested, according to the author. Enterovirus D68 was more prevalent in SARI cases than in ILI cases. Result: The presence of EV-D68 in acute respiratory infections in Ghana has been demonstrated for the first time in this review.
Source link: https://doi.org/10.4102/ajlm.v8i1.732
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