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A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Hepatitis C virus interacts with human platelet glycoprotein VI
Astrid Zahn1,2, Nicola Jennings2, Willem H Ouwehand1,2
1National Blood Service, Long Road, Cambridge CB2 2PT, UK.
The Journal of General Virology
|July 19, 2006
Summary
Hepatitis C virus (HCV) binds to human platelets via glycoprotein VI (GPVI). This interaction may facilitate viral transport to the liver, aiding HCV persistence.
Area of Science:
- Virology
- Immunology
- Hematology
Background:
- Hepatitis C virus (HCV) is known to interact with human platelets in vivo.
- Platelets may serve as a transport mechanism for infectious virions to the liver.
Purpose of the Study:
- To analyze the binding of native Hepatitis C virus (HCV) particles to platelet membrane glycoprotein VI (GPVI).
- To investigate the role of GPVI in HCV-mediated viral transport and persistence.
Main Methods:
- Pull-down assays and ELISA were used to analyze HCV and recombinant human GPVI (hD1D2) interaction.
- Binding inhibition assays with anti-hD1D2 antibodies were performed.
- Comparative analysis of human and murine D1D2 binding to HCV.
Main Results:
- Consistent interaction observed between HCV and recombinant human GPVI (hD1D2).
- Specific binding of 2-7% of HCV particles to hD1D2.
- Binding was dose-dependently inhibited by anti-hD1D2 antibodies, and human D1D2 showed significantly higher binding than murine D1D2, indicating specificity.
- Both D1 and D2 domains of GPVI are crucial for efficient HCV binding.
Conclusions:
- Glycoprotein VI (GPVI) acts as a platelet surface ligand for Hepatitis C virus (HCV).
- This interaction likely plays a role in the viral transport and persistence of HCV.
- Targeting the HCV-GPVI interaction could offer new therapeutic strategies.
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