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Understanding Enterovirus D68-Induced Neurologic Disease: A Basic Science Review.

Alison M Hixon1, Joshua Frost2, Michael J Rudy3

  • 1Medical Scientist Training Program, University of Colorado School of Medicine, Aurora, CO 80045, USA.

Viruses
|September 7, 2019
PubMed
Summary

Enterovirus D68 (EV-D68) is linked to acute flaccid myelitis (AFM) in children. Contemporary EV-D68 strains show increased neurovirulence compared to historical strains, supporting its role in AFM outbreaks.

Keywords:
acute flaccid myelitisenterovirus D68experimental modelsmouse modelsneuropathogenesisparalysis

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Area of Science:

  • Virology
  • Neurology
  • Epidemiology

Background:

  • The 2014 US epidemic of enterovirus D68 (EV-D68)-induced respiratory illness coincided with a rise in acute flaccid myelitis (AFM) in children.
  • AFM presents as a paralytic illness with similarities to poliomyelitis.
  • While a definitive causal link is pending, substantial evidence implicates EV-D68 in recent AFM outbreaks.

Purpose of the Study:

  • To review evidence from experimental models regarding the neurovirulence of contemporary EV-D68 strains.
  • To compare the characteristics of recent EV-D68 strains with historical ones.
  • To establish the biological plausibility of EV-D68 as a causative agent of AFM.

Main Methods:

  • Analysis of genomic sequences of contemporary and historical EV-D68 strains.
  • Assessment of receptor utilization by different EV-D68 strains.
  • In vitro studies on the ability of EV-D68 to infect neurons.
  • In vivo studies evaluating neuropathogenicity in mouse models.

Main Results:

  • Contemporary EV-D68 strains exhibit altered genomic sequences compared to historical strains.
  • Differences in receptor utilization and neuronal infection capabilities were observed.
  • Experimental models demonstrated increased neuropathogenicity of recent EV-D68 strains in mice.
  • EV-D68 strains from the 2014 outbreak and subsequent periods show enhanced neurovirulence factors.

Conclusions:

  • Experimental data provide biological plausibility for EV-D68 being a causal agent of AFM.
  • Contemporary EV-D68 strains possess distinct characteristics contributing to neurovirulence.
  • Established experimental models offer avenues for studying AFM pathogenesis and developing treatments.