Author/Authors :
Liu، Yuan نويسنده , , Zou، Ziying نويسنده Department of Microbiology and Immunology, Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China Zou, Ziying , Zhu، Bing نويسنده , , Hu، Zonghai نويسنده Department of Microbiology and Immunology, Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China Hu, Zonghai , Zeng، Ping نويسنده Department of Clinical Chemistry, Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China Zeng, Ping , Wu، Lijuan نويسنده Laboratory Medicine Center, General Hospital of Chengdu Military Region of PLA, Chengdu, China Wu, Lijuan
Abstract :
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 () was reported contributing to the production of interferon-β in macrophages. The aim of this study was to assess the role of in induction of IFN-β and inhibition of HCV infection in hepatocytes. Induction of IFN-β by in Huh7 and Huh7.5.1 was determined by real-time PCR and western blotting in vitro. Inhibition of HCV replication by overexpression in hepatocytes was assessed. increased the expression of IFN-β in hepatocytes with or without HCV infection. Induction of IFN-β by was enhanced with the presence of hepatitis C virus. Overexpression of in hepatocytes inhibited HCV replication. However, HCV infection did not regulate intracellular expression of . 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.
