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Extracellular Vesicle Release Promotes Viral Replication during Persistent HCV Infection
Yucel Aydin1, Ali Riza Koksal2, Venu Reddy1
1Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, LA 70112, USA.
Cells
|April 30, 2021
Summary
Hepatitis C virus (HCV) infection impairs autophagic degradation, promoting viral persistence via extracellular vesicle release. Blocking this release suppresses HCV replication and triggers immune responses, suggesting a novel antiviral strategy.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Hepatitis C virus (HCV) utilizes autophagy for replication but excessive autophagy can cause cell death.
- Previous work showed HCV stress inhibits autophagy via beclin 1 degradation.
- Mechanisms regulating secretory and degradative autophagy in persistent HCV infection remain unclear.
Purpose of the Study:
- To elucidate the mechanisms of viral persistence in the context of impaired degradative autophagy.
- To investigate the role of extracellular vesicle (EV) release in HCV survival and immune evasion.
Main Methods:
- Utilized CD63-green fluorescence protein (CD63-GFP) labeled Huh-7.5 cells for HCV infection studies.
- Analyzed autophagic degradation of CD63-GFP at early and late stages of HCV infection.
- Investigated the impact of blocking EV and exosome release on HCV replication and host cell viability.
Main Results:
- Early HCV infection induced autophagy, degrading CD63-GFP and favoring replication.
- Persistent HCV infection led to impaired autophagic degradation and CD63-GFP accumulation.
- Blocking EV/exosome release suppressed HCV replication without affecting cell viability and triggered interferon lambda 1 secretion.
Conclusions:
- Impaired autophagic degradation promotes EV/exosome release, facilitating HCV persistence.
- EV release acts as an innate immune escape mechanism for HCV.
- Inhibiting EV release presents a potential therapeutic strategy against HCV and other RNA viruses.
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