gga-miR-454 通过直接靶向 IBDV 基因组片段 B 和细胞因子信号转导抑制因子 6（SOCS6）来抑制传染性法氏囊病病毒（IBDV）的复制。
gga-miR-454 suppresses infectious bursal disease virus (IBDV) replication via directly targeting IBDV genomic segment B and cellular Suppressors of Cytokine Signaling 6 (SOCS6).
机构信息
State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China; Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China; Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, China Agricultural University, Beijing 100193, China; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
出版信息
Virus Res. 2018 Jul 2;252:29-40. doi: 10.1016/j.virusres.2018.05.015. Epub 2018 May 16.
MicroRNAs (miRNAs), as post-transcriptional regulators, play important roles in the process of viral infection through inhibiting virus replication or modulating host immune response. However, the role of miRNAs in host response against infectious bursal disease virus (IBDV) infection is still unclear. In this study, we found that gga-miR-454 of the host was decreased in response to IBDV infection and that transfection of DF-1 cells with miR-454 inhibited IBDV replication via directly targeting the specific sequence of IBDV genomic segment B, while blockage of endogenous miR-454 by inhibitors enhanced virus replication. Furthermore, gga-miR-454 increased the expression of IFN-β by targeting Suppressors of Cytokine Signaling 6 (SOCS6), enhancing the antiviral response of host cells. These findings highlight a crucial role of gga-miR-454 in host defense against IBDV infection.
微小 RNA（miRNAs）作为转录后调控因子，通过抑制病毒复制或调节宿主免疫反应，在病毒感染过程中发挥重要作用。然而，miRNAs 在宿主对传染性法氏囊病病毒（IBDV）感染的反应中的作用尚不清楚。在本研究中，我们发现宿主的gga-miR-454 对 IBDV 感染的反应降低，并且通过直接靶向 IBDV 基因组片段 B 的特定序列，DF-1 细胞中转染 miR-454 抑制 IBDV 复制，而通过抑制剂阻断内源性 miR-454 则增强病毒复制。此外，gga-miR-454 通过靶向细胞因子信号转导抑制因子 6（SOCS6）增加 IFN-β 的表达，增强宿主细胞的抗病毒反应。这些发现强调了 gga-miR-454 在宿主防御 IBDV 感染中的关键作用。
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