lrrfip1 inhibits hepatitis c virus replication by inducing type i interferon in hepatocytes

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.