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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, Indiana 47405-7102, United States.
ACS Infectious Diseases
|June 14, 2024
Summary
Reovirus capsids actively disrupt cell membranes, a cholesterol-dependent process that enhances viral entry and infection. This finding reveals the critical role of capsid-lipid interactions in nonenveloped virus infection.
Area of Science:
- Virology
- Cell Biology
- Biophysics
Background:
- Nonenveloped viruses require unique mechanisms to infect host cells.
- Understanding viral entry is key for developing antiviral therapies.
- The role of the viral capsid in membrane disruption is not fully understood.
Purpose of the Study:
- To elucidate the dynamic steps of reovirus capsid-mediated membrane disruption.
- To investigate the role of cholesterol in reovirus entry.
- To correlate membrane disruption with viral infectivity.
Main Methods:
- Live cell imaging to observe viral-host interactions.
- Model lipid membrane systems to study capsid-membrane dynamics.
- Analysis of viral variants with differing membrane disruption capabilities.
Main Results:
- Reovirus capsids actively deform and permeabilize lipid membranes.
- Cholesterol enhances reovirus capsid adsorption and pore formation.
- Capsid-induced membrane perturbations are more extensive than those caused by viral peptides.
- Membrane disruption extent correlates positively with viral infection efficiency.
Conclusions:
- Reovirus capsids play a direct, active role in breaching host cell membranes.
- Cholesterol homeostasis significantly influences nonenveloped virus entry.
- Capsid-lipid interactions are crucial for understanding viral infection dynamics and developing new antiviral strategies.
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