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Echoviruses bind heparan sulfate at the cell surface.
I G Goodfellow1, A B Sioofy, R M Powell
1Division of Virology, Institute of Biomolecular and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Journal of Virology
|April 20, 2001
Summary
Echoviruses (EV) can attach to cells independently of decay-accelerating factor (DAF). Heparan sulfate appears to be a key attachment molecule for EV infection, blocking viral entry.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Echoviruses (EV) are known to bind to host cells via decay-accelerating factor (DAF).
- Some EV strains exhibit DAF-independent cell binding to human and murine cells.
Purpose of the Study:
- To investigate the role of heparan sulfate in EV attachment and infection.
- To identify alternative cellular receptors for EV beyond DAF.
Main Methods:
- Radiolabeling of echoviruses for binding assays.
- Enzymatic pretreatment of cells with heparinase 1.
- Blocking experiments using heparin to inhibit viral binding and infection.
- Infection assays using various EV strains, including clinical isolates.
Main Results:
- Heparinase 1 and heparin treatment significantly blocked the binding of radiolabeled EV to cell surfaces.
- Heparin effectively prevented infection by specific EV types, including EV 6 clinical isolates and DAF-non-binding EV.
- These findings indicate a DAF-independent mechanism of EV cell attachment.
Conclusions:
- Heparan sulfate serves as a crucial attachment molecule for echovirus entry into host cells.
- This mechanism is relevant for EV strains that do not bind DAF, highlighting its importance in viral pathogenesis.