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Zika Virus Infectious Cell Culture System and the In Vitro Prophylactic Effect of Interferons
Published on: August 23, 2016
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A Novel Mechanism for Zika Virus Host-Cell Binding
Courtney A Rieder1, Jonathan Rieder1, Sebastién Sannajust1,2
1Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England; Armidale NSW 2351, Australia.
Viruses
|December 5, 2019
Summary
Zika virus (ZIKV) binding involves the E protein
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Zika virus (ZIKV) emerged in the Western Hemisphere with novel clinical presentations.
- Understanding ZIKV entry mechanisms is crucial for developing antiviral strategies.
Purpose of the Study:
- To identify putative binding mechanisms of ancestral and emergent ZIKV strains.
- To investigate the role of the E protein residue asparagine 154 (ASN154) and phosphatidylserine (PS) in ZIKV infection.
Main Methods:
- Synthetic peptides representing the ASN154 region of ZIKV strains were used to model E protein/cell interactions.
- Interactions were tested with neuronal cells, fibroblasts, MDCK, and Vero cells.
- Annexin V was used to assess the role of PS-mediated entry.
Main Results:
- Peptides containing ASN154 significantly bound to and inhibited infectivity in various cell types, including neuronal cells.
- This region represents a conserved binding mechanism for both African and Western Hemisphere ZIKV strains.
- Western Hemisphere strains may utilize PS-mediated entry as a secondary infection mechanism.
Conclusions:
- The region surrounding E protein ASN154 is critical for ZIKV binding to host cells, including neurons and fibroblasts.
- Phosphatidylserine-mediated entry appears to be an additional mechanism for Western Hemisphere ZIKV strains.
- These findings provide insights into ZIKV pathogenesis and potential therapeutic targets.
