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Abl Tyrosine Kinase Regulates Hepatitis C Virus Entry
Saehong Min1,2, Yun-Sook Lim2, Dongjo Shin1,3
1Department of Biomedical Gerontology, Graduate School of Hallym UniversityChuncheon, South Korea.
Frontiers in Microbiology
|July 5, 2017
Summary
Abl kinase is crucial for hepatitis C virus (HCV) propagation. Inhibiting Abl kinase with imatinib or dasatinib blocks HCV entry, suggesting Abl is a novel host factor for viral infection.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Abl is a key regulator of cellular processes like actin dynamics and proliferation.
- Hepatitis C virus (HCV) infection relies on host cell factors for its life cycle.
Purpose of the Study:
- To investigate the role of Abl kinase in hepatitis C virus (HCV) infection.
- To determine if Abl kinase activity is essential for HCV entry and propagation.
Main Methods:
- Knockdown of Abl expression in cultured cells.
- Treatment with Abl tyrosine kinase inhibitors (imatinib, dasatinib).
- HCV pseudoparticle infection assays, transferrin uptake, and immunofluorescence assays.
Main Results:
- Abl knockdown significantly impaired HCV propagation.
- Imatinib and dasatinib treatment reduced HCV RNA and protein levels.
- Abl kinase activity is necessary for HCV entry, specifically at the clathrin-mediated endocytosis step.
Conclusions:
- Abl kinase is a critical host factor required for efficient HCV entry.
- Targeting Abl kinase may offer a novel therapeutic strategy against HCV infection.
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