ArticleVirus evolution2016
Genetic changes found in a distinct clade of Enterovirus D68 associated with paralysis during the 2014 outbreak.
Article in Virus evolution, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Epidemiological and Clinical Characteristics of the Enterovirus D68 Outbreak in Spain in 2024.Journal of medical virology · 2026Article
- Article
- Global Prevalence of Non-Polio Enteroviruses Pre- and Post COVID-19 Pandemic.Microorganisms · 2025Review
- Structural insights from vaccine candidates for EV-D68.Communications biology · 2025Article
- Platelet factor 4-derived C15 peptide broadly inhibits enteroviruses by disrupting viral attachment.Journal of virology · 2025Article
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- Structure-Based Lead Optimization of Enterovirus D68 2A Protease Inhibitors.Journal of medicinal chemistry · 2023Article
- Clinical and molecular epidemiologic features of enterovirus D68 infection in children with acute lower respiratory tract infection in China.Archives of virology · 2023Review
- RNA Structure in the 5' Untranslated Region of Enterovirus D68 Strains with Differing Neurovirulence Phenotypes.Viruses · 2023Article
- Is it time to switch to a formulation other than the live attenuated poliovirus vaccine to prevent poliomyelitis?Frontiers in public health · 2023Review
- Animal Models of Enterovirus D68 Infection and Disease.Journal of virology · 2022Review
- Role of branched-chain amino acid metabolism in the pathogenesis of obesity and type 2 diabetes-related metabolic disturbances BCAA metabolism in type 2 diabetes.Nutrition & diabetes · 2022Review
- Enterovirus D68 epidemic, UK, 2018, was caused by subclades B3 and D1, predominantly in children and adults, respectively, with both subclades exhibiting extensive genetic diversity.Microbial genomics · 2022Article
- Off-season circulation and characterization of enterovirus D68 with respiratory and neurological presentation using whole-genome sequencing.Frontiers in microbiology · 2022Article
- The pathogenesis and virulence of enterovirus-D68 infection.Virulence · 2021Review
- 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
- Non-Polio Enteroviruses from Acute Flaccid Paralysis Surveillance in Korea, 2012-2019.Viruses · 2021Article
- Epidemiology and Sequence-Based Evolutionary Analysis of Circulating Non-Polio Enteroviruses.Microorganisms · 2020Review
- Article
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11 authors.
Funding
Abstract
Enterovirus D68 (EV-D68) caused a severe respiratory illness outbreak in the United States in 2014. Reports of acute flaccid myelitis (AFM)/paralysis (AFP) in several independent epidemiological clusters of children with detectable EV-D68 have raised concerns that genetic changes in EV-D68 could be causing increased disease severity and neurological symptoms. To explore the potential link between EV-D68 genetic variations and symptom changes, we performed a series of comparative genomic analyses of EV-D68 2014 outbreak isolate sequences using data and analytical tools in the Virus Pathogen Resource (ViPR; www.viprbrc.org). Our results suggest that (1) three distinct lineages of EV-D68 were co-circulating in 2013 and 2014; (2) isolates associated with AFM/AFP belong to a single phylogenetic subclade - B1; (3) the majority of isolates from the B1 subclade have 21 unique substitutions that distinguish them from other isolates, including amino acid substitutions in the VP1, VP2, and VP3 capsid proteins and the 3D RNA-dependent RNA polymerase, and nucleotide substitutions in the internal ribosome entry sequence (IRES); (4) at 12 of these positions, B1 isolates carry the same residues observed at equivalent positions in paralysis-causing enteroviruses, including poliovirus, EV-D70 and EV-A71. Based on these results, we hypothesize that unique B1 substitutions may be responsible for the apparent increased incidence of neuropathology associated with the 2014 outbreak.
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