Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 296, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jbc.2021.100317
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Funding
- National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke [5K12NS098482-03]
- NIH/National Institute of Allergy and Infectious Diseases [R01AI148049]
- Johns Hopkins University Catalyst Award
- [HHSN272201700024I]
- [HHSN27220 1400007C]
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EV-D68 has evolved from a rare respiratory virus to a widespread pathogen causing severe respiratory illness and acute flaccid myelitis in children globally. Research on the molecular features and interaction with host cells has progressed, highlighting the need for further exploration of its pathogenic mechanisms.
In recent years, enterovirus D68 (EV-D68) has advanced from a rarely detected respiratory virus to a widespread pathogen responsible for increasing rates of severe respiratory illness and acute flaccid myelitis (AFM) in children worldwide. In this review, we discuss the accumulating data on the molecular features of EV-D68 and place these into the context of enterovirus biology in general. We highlight similarities and differences with other enteroviruses and genetic divergence from own historical prototype strains of EV-D68. These include changes in capsid antigens, host cell receptor usage, and viral RNA metabolism collectively leading to increased virulence. Furthermore, we discuss the impact of EV-D68 infection on the biology of its host cells, and how these changes are hypothesized to contribute to motor neuron toxicity in AFM. We highlight areas in need of further research, including the identification of its primary receptor and an understanding of the pathogenic cascade leading to motor neuron injury in AFM. Finally, we discuss the epidemiology of the EV-D68 and potential therapeutic approaches.
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