Cellular microRNA miR-26a suppresses replication of porcine reproductive and respiratory syndrome virus by activating innate antiviral immunity.
Cellular microRNA miR-26a suppresses replication of porcine reproductive and respiratory syndrome virus by activating innate antiviral immunity.
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DOI：
10.1038/srep10651
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发表时间：
2015-05-27
影响因子：
4.6
通讯作者：
Liu W
中科院分区：
文献类型：
--
作者：
Jia X;Bi Y;Li J;Xie Q;Yang H;Liu W
猪繁殖与呼吸综合征（PRRS）是近年来引起养猪业巨大经济损失的疾病。目前的PRRS疫苗未能有效预防和控制这种疾病。因此，需要开发新的抗病毒策略。microRNA在复杂的宿主-病原体相互作用网络中起着关键作用，但在PRRS病毒（PRRSV）感染过程中miRNAs的参与还没有得到很好的理解。在本研究中，miR-26 a预处理可显著抑制MARC-145细胞中的PRRSV复制并缓解细胞病变效应，并且这种抗病毒效应可持续至少120 h。荧光素酶报告基因分析表明，PRRSV基因组不是miRNA-26 a的靶基因。相反，RNA-seq分析表明，miR-26 a显著上调先天性抗病毒反应，包括激活I型干扰素（IFN）信号通路和促进IFN刺激基因的产生。这些发现表明，miR-26 a的递送可能为抗PRRSV治疗提供潜在的策略。
Porcine reproductive and respiratory syndrome (PRRS) has caused large economic losses in the swine industry in recent years. Current PRRS vaccines fail to effectively prevent and control this disease. Consequently, there is a need to develop new antiviral strategies. MicroRNAs play critical roles in intricate host-pathogen interaction networks, but the involvement of miRNAs during PRRS virus (PRRSV) infection is not well understood. In this study, pretreatment with miR-26a induced a significant inhibition of PRRSV replication and remission of the cytopathic effect in MARC-145 cells, and this antiviral effect was sustained for at least 120 h. Luciferase reporter analysis showed that the PRRSV genome was not the target of miRNA-26a. Instead, RNA-seq analysis demonstrated that miR-26a significantly up-regulated innate anti-viral responses, including activating the type I interferon (IFN) signaling pathway and promoting the production of IFN-stimulated genes. These findings suggest that delivery of miR-26a may provide a potential strategy for anti-PRRSV therapies.
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