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Enterovirus D68 molecular and cellular biology and pathogenesis
Matthew J Elrick1, Andrew Pekosz2, Priya Duggal3
1Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
The Journal of Biological Chemistry
|January 23, 2021
Summary
Enterovirus D68 (EV-D68) is a growing threat, causing severe respiratory illness and acute flaccid myelitis (AFM) in children. This review examines EV-D68
Area of Science:
- Virology
- Infectious Diseases
- Neuroscience
Background:
- Enterovirus D68 (EV-D68) has emerged as a significant global pathogen.
- EV-D68 is associated with severe respiratory illness and acute flaccid myelitis (AFM) in children.
- Understanding EV-D68's evolution and pathogenicity is crucial.
Purpose of the Study:
- To review the molecular characteristics of EV-D68.
- To contextualize EV-D68 within general enterovirus biology.
- To explore EV-D68's impact on host cells and motor neuron toxicity in AFM.
Main Methods:
- Review of accumulating data on EV-D68 molecular features.
- Comparative analysis with other enteroviruses and historical EV-D68 strains.
- Discussion of host cell interactions and hypothesized mechanisms of neurotoxicity.
Main Results:
- EV-D68 exhibits genetic divergence from historical strains, affecting capsid antigens and receptor usage.
- Changes in EV-D68 contribute to increased virulence and potential for motor neuron damage.
- Host cell biology is significantly impacted by EV-D68 infection.
Conclusions:
- EV-D68's evolving molecular features enhance its virulence.
- Further research is needed to identify EV-D68's primary receptor and clarify AFM pathogenesis.
- Understanding EV-D68 epidemiology and developing therapeutics are critical next steps.
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