Abstract:
BACKGROUND:Hepatitis C virus infection is one of the leading causes of end stage liver diseases. The innate immune response slows down viral replication by activating cytokines such as type I interferon (IFN-α/β), which trigger the synthesis of antiviral proteins and modulate the adaptive immune system. Recently, leucine-rich repeat (in Flightless I) interacting protein-1 (LRRFIP1) was reported contributing to the production of interferon-β in macrophages. OBJECTIVES:The aim of this study was to assess the role of LRRFIP1 in induction of IFN-β and inhibition of HCV infection in hepatocytes. MATERIALS AND METHODS:Induction of IFN-β by LRRFIP1 in Huh7 and Huh7.5.1 was determined by real-time PCR and western blotting in vitro. Inhibition of HCV replication by LRRFIP1 overexpression in hepatocytes was assessed. RESULTS:LRRFIP1 increased the expression of IFN-β in hepatocytes with or without HCV infection. Induction of IFN-β by LRRFIP1 was enhanced with the presence of hepatitis C virus. Overexpression of LRRFIP1 in hepatocytes inhibited HCV replication. However, HCV infection did not regulate intracellular expression of LRRFIP1. CONCLUSIONS:LRRFIP1 and its mediated production of type I interferon play a role in controlling HCV infection. The findings of this study provide new target for HCV treatment and contribute to development of anti-HCV drugs.
journal_name
Hepat Monjournal_title
Hepatitis monthlyauthors
Liu Y,Zou Z,Zhu B,Hu Z,Zeng P,Wu Ldoi
10.5812/hepatmon.15(5)2015.28473subject
Has Abstractpub_date
2015-05-23 00:00:00pages
e28473issue
5eissn
1735-143Xissn
1735-3408journal_volume
15pub_type
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