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10.5812/hepatmon.15(5)2015.28473

http://scihub22266oqcxt.onion/10.5812/hepatmon.15(5)2015.28473
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C4451274!4451274!26045710
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suck abstract from ncbi


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pmid26045710      Hepat+Mon 2015 ; 15 (5): ä
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  • LRRFIP1 Inhibits Hepatitis C Virus Replication by Inducing Type I Interferon in Hepatocytes #MMPMID26045710
  • Liu Y; Zou Z; Zhu B; Hu Z; Zeng P; Wu L
  • Hepat Mon 2015[May]; 15 (5): ä PMID26045710show ga
  • 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-?/?), 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-? in macrophages. Objectives:: The aim of this study was to assess the role of LRRFIP1 in induction of IFN-? and inhibition of HCV infection in hepatocytes. Materials and Methods:: Induction of IFN-? 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-? in hepatocytes with or without HCV infection. Induction of IFN-? 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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