LRRFIP1 Inhibits Hepatitis C Virus Replication by Inducing Type I Interferon in Hepatocytes |
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Authors: | Yuan Liu Ziying Zou Bing Zhu Zonghai Hu Ping Zeng Lijuan Wu |
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Institution: | 1.Department of Microbiology and Immunology, Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China;2.Department of Clinical Chemistry, Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China;3.Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China |
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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. |
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Keywords: | LRRFIP1 Protein Human Hepacivirus Interferon Type I |
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