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lüll Modulation of miR-122 on persistently Borna disease virus infected human oligodendroglial cells Qian J; Zhai A; Kao W; Li Y; Song W; Fu Y; Chen X; Zhang Q; Wu J; Li H; Zhong Z; Ling H; Zhang FAntiviral Res 2010[Aug]; 87 (2): 249-56Using RNAhybrid software we found the predicted binding of complementary sequences between miR-122 and viral mRNAs, may be important for the antiviral effect of miR-122 on Borna disease virus (BDV). A moderate expression of miR-122 was identified in human oligodendroglial cells (OL), but with a much lower level of miR-122 in BDV persistent infection (OL/BDV) and cells transfected with BDV gene expression vectors. Over-expression of miR-122 and specific blocking experiments demonstrated that miR-122 was able to specifically inhibit BDV protein synthesis, viral gene replication and transcription, and induce the secretion/synthesis of interferon (IFN) in OL and OL/BDV cells. The abolishment of miR-122 by AMO-122 inhibited endogenous IFN induction by IFN-beta. These results indicate that miR-122 can exert direct antiviral function by inhibiting BDV translation and replication on one hand, while acting indirectly through IFN to increase the host innate immunity to modulate the virus-host interactions on the other hand.|Borna disease virus/*immunology/*isolation & purification[MESH]|Gene Expression Profiling[MESH]|Humans[MESH]|Interferons/metabolism[MESH]|MicroRNAs/*biosynthesis/*genetics/immunology[MESH]|Nucleic Acid Hybridization[MESH]|Oligodendroglia/*immunology/*virology[MESH]|Viral Proteins/biosynthesis[MESH] |