Premium
Micro RNA ‐130a inhibits HCV replication by restoring the innate immune response
Author(s) -
Li S.,
Duan X.,
Li Y.,
Liu B.,
McGilvray I.,
Chen L.
Publication year - 2014
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.12131
Subject(s) - innate immune system , replicon , hepatitis c virus , virology , interferon , biology , immune system , tlr3 , rig i , viral replication , ribavirin , tlr7 , rna interference , rna , immunology , cancer research , virus , gene , toll like receptor , genetics , plasmid
Summary Hepatitis C virus ( HCV ) infection is a major cause of chronic hepatitis and hepatocellular carcinoma. Currently pegylated interferon ( IFN ) combined with ribavirin remains the best therapeutic approach, although patients infected with HCV genotype I may benefit from adding protease inhibitors as ‘triple therapy’. Micro RNA s (mi RNA s) are endogenous small noncoding RNA s that regulate gene expression and have recently been shown to play an important role in human innate immune response and as an antiviral in chimpanzees. We studied the effect of miR‐130a on the HCV replication. We found that miR‐130a significantly inhibits HCV replication in both HCV replicon and J6‐/ JFH 1‐infected cells. Over expression of miR‐130a upregulated the expression of type I IFN ( IFN ‐α/ IFN ‐β), ISG 15, USP 18 and MxA, which are involved in innate immune response and decreased expression of miR‐122, a well‐defined mi RNA promoting HCV production. In conclusion, miR‐130a inhibits HCV replication/production by restoring host innate immune responses and/or downregulating pro‐ HCV miR‐122. miR‐130a might be a potential drug target by modulating host innate immune responses to combat HCV infection.