The Molecular Mechanism Of Gga-miR-155 Inhibits The Replication Of Infectious Bursal Disease Virus

Infeetious bursal disease virus(IBDV), the etiological agent of Infectious disease, causes severe immunodepression of Beellresponse in chickens, mainly at the ages of 3-6 weeks, by destruction of lymphocytes in the bursa of Fabricius. The appeared and spread of IBDV in our country causing sever economic losses. microRNA is a kind of small non-coding RNA, with length of 21 to 25 nt, which could degrade the target gene mRNA at post-transcription to inhibit translation and has a key role of physiological and pathological process. Significant expression difference of gga-miRNA-155 was detected in IBDV infected CEF or SPF chicken. This paper explore the molecular mechanism of gga-miR-155 influenced the replication of IBDV by means of molecular biology technique and bioinformatics methods such as luciferase assays, wetern blot, qRT-PCR etc. The result was summarized as follow:1. Explore the effection of gga-miR-155 in replication of IBDV and IFN secretionFirstly, the gga-miR-155 mimics were synthesized and transfected into DF-1 cells, qRT-PCR and TCID50 analysis indicated gga-miR-155 inhibitely the replication of IBDV. Futhermore to explore the moleculer mechanism of the gga-miR-155 in inhibiting replication of IBDV, IFN analysis indicated the type I IFN production was enhanced. So gga-miR-155 inhibitely regulated IBDV-triggered the innate immunity.2. Bioinformatics analysis of gga-miR-155 inhibite the replication of IBDV.Secondly, analyse the target gene of gga-miR-155 with bioinformatics. We choose the SOCS1 from these target genes in the miRDB. SOCS1 is a negative regulate factor of signal transduction processes, which has important role of innate immunity and adaptive immunity. Then, confirmed it by means of the Luciferase assays and wetern blot at mRNA level and protein level. Western blot analysis and real-time RT-PCR showed that the SOCS1 protein level and mRNA level were significantly higher in the IBDV infected gga-miR-155-transfected-DF-1 cells than that in DF-1 cells. The results indicated that gga-miR-155 up-regulated SOCS1 expression at the transcription levels. Therefore, we demonstrate that inducible gga-miR-155 feedback negatively regulates host antiviral innate immune response by promoting type I IFN signaling via targeting SOCS1. This paper lay the foundation of explore new antiviral drugs and the targets of immune molecules for the prevention and control of IBDV.