ArticlePloS one2015
Analysis of Enterovirus 68 Strains from the 2014 North American Outbreak Reveals a New Clade, Indicating Viral Evolution.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed.
- Enterovirus D68 B3 clade strains are efficiently recovered from cDNA infectious clones in 293T cells and infect human spinal cord organoids.Journal of virology · 2026Article
- Prevalence and epidemiology of enterovirus species in a pediatric oncology patient population.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2025Article
- Enterovirus A71 priorities, challenges, and future opportunities in humoral immunity and vaccine development.NPJ vaccines · 2025Review
- Enterovirus D68: Genomic and Clinical Comparison of 2 Seasons of Increased Viral Circulation and Discrepant Incidence of Acute Flaccid Myelitis-Maryland, USA.Open forum infectious diseases · 2024Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Identification of four neutralizing antigenic sites on the enterovirus D68 capsid.Journal of virology · 2023Article
- Evolution, geographic spreading, and demographic distribution of Enterovirus D68.PLoS pathogens · 2022Article
- The pathogenesis and virulence of enterovirus-D68 infection.Virulence · 2021Review
- Complete Genome Sequences of Enterovirus D68 Clade A and D Strains in the Philippines.Microbiology resource announcements · 2021Article
- Retrospective Study of the Upsurge of Enterovirus D68 Clade D1 among Adults (2014-2018).Viruses · 2021Article
- Article
- Unraveling the Mysteries of Acute Flaccid Myelitis: Scientific Opportunities and Priorities for Future Research.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- Article
- Review
- Review
- Molecular epidemiological study of enterovirus D68 in hospitalised children in Hong Kong in 2014-2015 and their complete coding sequences.BMJ open respiratory research · 2019Article
- Review
- Divergent Pathogenic Properties of Circulating Coxsackievirus A6 Associated with Emerging Hand, Foot, and Mouth Disease.Journal of virology · 2018Article
- The association between acute flaccid myelitis (AFM) and Enterovirus D68 (EV-D68) - what is the evidence for causation?Euro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2018Review
- First Report of a Fatal Case Associated with EV-D68 Infection in Hong Kong and Emergence of an Interclade Recombinant in China Revealed by Genome Analysis.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 68 (EVD68) causes respiratory illness, mostly in children. Despite a reported low-level of transmission, the occurrence of several recent outbreaks worldwide including the 2014 outbreak in North America has raised concerns regarding the pathogenesis and evolution of EVD68. To elucidate the phylogenetic features of EVD68 and possible causes for the 2014 outbreak, 216 EVD68 strain sequences were retrieved from Genbank, including 22 from the 2014 outbreak. Several geographic and genotypic origins were established for these 22 strains, 19 of which were classified as Clade B. Of these 19 strains, 17 exhibited subsequent clustering and variation in protein residues involved in host-receptor interaction and/or viral antigenicity. Approximately 18 inter-clade variations were detected in VP1, which led to the identification of a new Clade D in EVD68 strains. The classification of this new clade was also verified by the re-construction of a Neighbor-Joining tree during the phylogenetic analysis. In addition, our results indicate that members of Clade B containing highly specific alterations in VP1 protein residues were the foremost contributors to the 2014 outbreak in the US. Altered host-receptor interaction and/or host immune recognition may explain the evolution of EVD68 as well as the global emergence and ongoing adaptation of this virus.
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