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Mapping Attenuation Determinants in Enterovirus-D68.

Ming Te Yeh1, Sara Capponi2,3, Adam Catching1,4

  • 1Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94158, USA.

Viruses
|August 14, 2020
PubMed
Summary
This summary is machine-generated.

Enterovirus D68 (EV-D68) causes paralysis. A specific mutation in the VP3 protein (Isoleucine to Valine at position 88) significantly reduced viral neurovirulence in a mouse model.

Keywords:
VP3enterovirusenterovirus-D68infectious clonesmouse modelparalysisvirulence determinant

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Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Enterovirus D68 (EV-D68) outbreaks occurred in the US in 2014, 2016, and 2018.
  • EV-D68 is linked to neurological disease, including paralysis, in humans.

Purpose of the Study:

  • To identify genetic determinants of EV-D68 virulence.
  • To understand the mechanisms underlying EV-D68-induced paralysis.

Main Methods:

  • Neonatal type I interferon receptor knockout mice were used as a model for EV-D68 infection.
  • Comparative sequence analysis of virulent and attenuated EV-D68 strains.
  • Construction of chimeric and point-mutated infectious viral clones.

Main Results:

  • The mouse model recapitulated human EV-D68-associated paralysis and death.
  • Specific genetic changes were conserved among virulent strains, including mutations in the 5'-UTR, VP3, VP1, 2A, and 3A.
  • A single amino acid substitution (Isoleucine to Valine at position 88 in VP3) attenuated neurovirulence.

Conclusions:

  • The VP3 protein plays a critical role in EV-D68 neurovirulence.
  • The identified mutation significantly reduces viral replication in the central nervous system.
  • This finding provides insights into EV-D68 pathogenesis and potential therapeutic targets.