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Updated: Jul 13, 2025

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In Vitro Disassembly of Influenza A Virus Capsids by Gradient Centrifugation
Published on: March 27, 2016
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Enterovirus D68 capsid formation and stability requires acidic compartments
Ganna Galitska1, Alagie Jassey1, Michael A Wagner1
1Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, Maryland, USA.
Mbio
|October 11, 2023
Summary
Enterovirus D68, a cause of childhood paralysis, needs acidic environments for viral assembly. Blocking acidification may offer new treatments for enterovirus diseases.
Area of Science:
- Virology
- Molecular Biology
- Pathogenesis
Background:
- Enterovirus D68 causes acute flaccid myelitis, a paralytic illness in children.
- Poliovirus, a related picornavirus, utilizes acidic environments for host-to-host transmission.
- Previous research indicated poliovirus requires acidic compartments for particle maturation.
Purpose of the Study:
- To investigate the role of acidic intracellular compartments in Enterovirus D68 (EV-D68) lifecycle.
- To compare the acidification requirements of EV-D68 with poliovirus.
- To explore potential therapeutic strategies targeting enterovirus acidification dependence.
Main Methods:
- Cell culture models to study EV-D68 replication.
- Acidification assays to monitor intracellular pH.
- Viral particle assembly and stability experiments.
- Analysis of viral maturation processes.
Main Results:
- Enterovirus D68 requires acidic intracellular vesicles for viral assembly.
- EV-D68 also needs acidic compartments for maintaining viral particle integrity.
- Unlike poliovirus, EV-D68's acidification dependence occurs at an earlier stage (assembly).
Conclusions:
- Acidic intracellular compartments are critical for Enterovirus D68 assembly and stability.
- These findings suggest that targeting cellular acidification could be a viable strategy against EV-D68 infections.
- The distinct acidification requirements highlight differences in picornavirus replication strategies.
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