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Hepatitis C Virus Driven AXL Expression Suppresses the Hepatic Type I Interferon Response
Scott A Read1, Enoch S Tay1, Mahsa Shahidi1
1Storr Liver Centre, Westmead Millennium Institute, University of Sydney at Westmead Hospital, Westmead, Australia.
Plos One
|August 28, 2015
Summary
Hepatitis C virus (HCV) infection is linked to the immune system. Elevated AXL in the liver may cause interferon refractoriness, hindering viral clearance in patients with specific genotypes.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Hepatitis C virus (HCV) infection clearance depends on the hepatic innate immune system.
- Interferon (IFN) stimulated genes (ISGs) activation indicates interferon refractoriness, reducing treatment efficacy.
- AXL, a receptor tyrosine kinase, regulates IFN signaling but its role in HCV is unexplored.
Purpose of the Study:
- Investigate AXL's role in HCV infection and its impact on IFN-mediated antiviral responses.
- Determine if AXL expression correlates with interferon refractoriness and treatment outcomes in chronic HCV patients.
Main Methods:
- Studied AXL expression in HCV-infected cells (in vitro) and patients (in vivo).
- Assessed AXL's effect on IFNα-mediated ISG expression and antiviral activity against HCV.
- Correlated AXL expression levels with IFNL3 rs12979860 genotypes and IFN treatment response.
Main Results:
- AXL is upregulated by HCV infection, type I/III IFNs, and inflammatory pathways.
- AXL inhibits IFNα-induced ISG expression, reducing antiviral efficacy against HCV.
- Lower AXL liver expression and higher blood AXL induction were observed in patients with favorable IFNL3 genotypes post-IFN treatment.
Conclusions:
- Elevated hepatic AXL expression may contribute to interferon refractoriness in chronic HCV.
- AXL could be a key factor in the unfavorable rs12979860 genotype's association with lower viral clearance rates.
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