Enterovirus D68 molecular and cellular biology and pathogenesis
| Autor: | Priya Duggal, Andrew Pekosz, Matthew J. Elrick |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Reviews Virulence Context (language use) ICAM intercellular adhesion molecule Biology NCS nerve conduction study medicine.disease_cause Biochemistry CDC US Centers for Disease Control and Prevention 03 medical and health sciences MDA melanoma differentiation–associated protein RIG retinoic acid–inducible gene medicine Enterovirus Infections Humans hnRNP heterogenous nuclear ribonucleoprotein AFM acute flaccid myelitis innate immunity Molecular Biology virus replication Phylogeny COVID-19 coronavirus disease 2019 EV-A71 enterovirus A71 Enterovirus D Human Toll-like receptor eIF4 eukaryotic initiation factor 4 Innate immune system 030102 biochemistry & molecular biology enterovirus EMG electromyography study adaptive immunity Cell Biology Neuromuscular Diseases Myelitis GI gastrointestinal Acquired immune system Acute flaccid myelitis IVIG intravenous immunoglobulin 030104 developmental biology IRES internal ribosome entry site iPS induced pluripotent stem cell Immunology EV-D68 enterovirus D68 Central Nervous System Viral Diseases acute flaccid myelitis Enterovirus Respiratory virus TLR Toll-like receptor |
| Zdroj: | The Journal of Biological Chemistry |
| ISSN: | 1083-351X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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