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Cholesterol-Dependent Membrane Deformation by Metastable Viral Capsids Facilitates Entry
Mengchi Jiao1, Pranav Danthi2, Yan Yu1
1Department of Chemistry, Indiana University, Bloomington, IN 47405-7102.
Biorxiv : the Preprint Server for Biology
|January 23, 2024
Summary
Non-enveloped viruses, like reovirus, actively disrupt host cell membranes using their capsids, not just peptides. This cholesterol-dependent process enhances viral infection efficiency.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Non-enveloped viruses require specific mechanisms to enter host cells.
- Current understanding suggests membrane lytic peptides are key, but the viral capsid's role is unclear.
Approach:
- Directly observed reovirus capsid interactions with lipid membranes in live cells and model systems.
- Investigated the role of cholesterol in capsid-mediated membrane disruption.
Key Points:
- Reovirus capsids actively deform and permeabilize cholesterol-dependent lipid membranes.
- Capsids induce extensive membrane perturbations, including budding, bridging, and rupture.
- Cholesterol enhances capsid adsorption and pore formation, influencing infection efficiency.
Conclusions:
- Viral capsids play a direct, active role in non-enveloped virus entry by disrupting host membranes.
- Cholesterol homeostasis significantly impacts viral infection dynamics through capsid-lipid interactions.
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