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Exosomes promote caprine parainfluenza virus type 3 infection by inhibiting autophagy.
Journal of General Virology ( IF 3.8 ) Pub Date : 2020-07-01 , DOI: 10.1099/jgv.0.001424
Li Mao 1, 2 , Panhong Liang 2 , Wenliang Li 1, 3 , Shaohua Zhang 2 , Maojun Liu 1, 4 , Leilei Yang 1 , Jizong Li 1 , Huixia Li 2 , Fei Hao 1 , Min Sun 1 , Wenwen Zhang 1 , Liqun Wang 2 , Xuepeng Cai 2 , Xuenong Luo 2, 5
Affiliation  

Caprine parainfluenza virus type 3 (CPIV3) is a novel important pathogen causing respiratory disease in goats, but the pathogenic mechanism is not clear yet. Evidence suggests that exosomes transfer biologically active molecules between cells. Viral infections can cause profound changes in exosome components, and exosomes have been involved in viral transmission and pathogenicity. In this study, we explored the characteristics and functions of exosomes purified from the supernatant of Madin–Darby bovine kidney (MDBK) cells inoculated with CPIV3. Infection of CPIV3 showed increased exosome secretion and the loading of viral proteins and RNA into exosomes. These exosomes were capable of transferring CPIV3 genetic materials to recipient cells to establish a productive infection and promote the viral replication. To explore the potential mechanism, small RNA deep sequencing revealed that CPIV3 exosomes contained a diverse range of RNA species, including miRNA and piRNA, in proportions different from exosomes isolated from mock-infected cells. Expression patterns of 11 differentially expressed miRNAs were subsequently validated by quantitative reverse transcriptase PCR (qRT-PCR). Targets of miRNAs were predicted and functional annotation analysis showed that the main pathways involved were autophagy signalling ways. Autophagy inhibited by the CPIV3-exosome was further verified, and miR-126–3 p_2 packaged in the vesicles was an important regulation factor in this process. Inhibition of autophagy may be one of the responsible reasons for promoting efficient replication of exosome-mediated CPIV3 infection. The study suggests that exosomes are key in pathogenesis or protection against CPIV3. Further understating of their role in CPIV3 infection may bring novel insight to the development of protection measures.

中文翻译:

外来体通过抑制自噬促进了3型山羊副流感病毒感染。

山羊副流感病毒3型(CPIV3)是引起山羊呼吸系统疾病的一种新型重要病原体,但其致病机理尚不清楚。有证据表明,外泌体在细胞之间转移生物活性分子。病毒感染可引起外泌体成分发生深刻变化,并且外泌体已参与病毒的传播和致病性。在这项研究中,我们探讨了从用CPIV3接种的Madin-Darby牛肾(MDBK)细胞上清液中纯化的外泌体的特性和功能。CPIV3感染显示出外泌体分泌增加,病毒蛋白和RNA进入外泌体。这些外泌体能够将CPIV3遗传物质转移至受体细胞,以建立生产性感染并促进病毒复制。为了探索潜在的机制,小RNA深度测序表明,CPIV3外泌体包含的RNA种类繁多,包括miRNA和piRNA,其比例不同于从模拟感染细胞中分离出的外泌体。随后通过定量逆转录酶PCR(qRT-PCR)验证了11种差异表达的miRNA的表达模式。预测了miRNA的靶标,功能注释分析表明所涉及的主要途径是自噬信号传导途径。进一步验证了CPIV3-外来体抑制的自噬,包装在囊泡中的miR-126–3 p_2是该过程中的重要调节因子。抑制自噬可能是促进外泌体介导的CPIV3感染有效复制的原因之一。该研究表明,外泌体在发病机理或针对CPIV3的保护中起关键作用。
更新日期:2020-08-20
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