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微小 RNA 在宿主防御传染性法氏囊病病毒 (IBDV) 感染中的作用:一个隐藏的前线。

Role of MicroRNAs in Host Defense against Infectious Bursal Disease Virus (IBDV) Infection: A Hidden Front Line.

机构信息

Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.

出版信息

Viruses. 2020 May 14;12(5):543. doi: 10.3390/v12050543.

DOI:10.3390/v12050543
PMID:32423052
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7291112/
Abstract

Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by infectious bursal disease virus (IBDV). In recent years, remarkable progress has been made in the understanding of the pathogenesis of IBDV infection and the host response, including apoptosis, autophagy and the inhibition of innate immunity. Not only a number of host proteins interacting with or targeted by viral proteins participate in these processes, but microRNAs (miRNAs) are also involved in the host response to IBDV infection. If an IBDV-host interaction at the protein level is taken imaginatively as the front line of the battle between invaders (pathogens) and defenders (host cells), their fight at the RNA level resembles the hidden front line. miRNAs are a class of non-coding single-stranded endogenous RNA molecules with a length of approximately 22 nucleotides (nt) that play important roles in regulating gene expression at the post-transcriptional level. Insights into the roles of viral proteins and miRNAs in host response will add to the understanding of the pathogenesis of IBDV infection. The interaction of viral proteins with cellular targets during IBDV infection were previously well-reviewed. This review focuses mainly on the current knowledge of the host response to IBDV infection at the RNA level, in particular, of the nine well-characterized miRNAs that affect cell apoptosis, the innate immune response and viral replication.

摘要

传染性法氏囊病(IBD)是一种由传染性法氏囊病病毒(IBDV)引起的急性、高度接触传染性和免疫抑制性禽类疾病。近年来,人们对 IBDV 感染的发病机制和宿主反应有了更深入的了解,包括细胞凋亡、自噬和固有免疫抑制。不仅有许多与病毒蛋白相互作用或作为病毒蛋白靶标的宿主蛋白参与了这些过程,而且 microRNAs(miRNAs)也参与了宿主对 IBDV 感染的反应。如果将病毒-宿主相互作用在蛋白质水平上想象为入侵者(病原体)和防御者(宿主细胞)之间战斗的前线,那么它们在 RNA 水平上的斗争就类似于隐藏的前线。miRNAs 是一类长度约为 22 个核苷酸(nt)的非编码单链内源性 RNA 分子,在转录后水平上对基因表达具有重要的调控作用。深入了解病毒蛋白和 miRNAs 在宿主反应中的作用将有助于理解 IBDV 感染的发病机制。先前已经很好地综述了 IBDV 感染期间病毒蛋白与细胞靶标的相互作用。本综述主要关注宿主对 IBDV 感染的 RNA 水平反应的最新知识,特别是影响细胞凋亡、固有免疫反应和病毒复制的 9 种特征明确的 miRNAs。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/7291112/e62be5d3813c/viruses-12-00543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/7291112/e62be5d3813c/viruses-12-00543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/7291112/e62be5d3813c/viruses-12-00543-g001.jpg

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miR-454 performs tumor-promoting effects in oral squamous cell carcinoma via reducing NR3C2.miR-454 通过降低 NR3C2 促进口腔鳞状细胞癌的肿瘤发生。
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microRNA-454 promotes liver tumor-initiating cell expansion by regulating SOCS6.
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The long noncoding RNA loc107053557 acts as a gga-miR-3530-5p sponge to suppress the replication of vvIBDV through regulating STAT1 expression.长链非编码 RNA loc107053557 作为 gga-miR-3530-5p 的海绵体,通过调节 STAT1 表达来抑制 vvIBDV 的复制。
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