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在VSV感染的BHK-21细胞中对长非编码RNA和mRNA资料的转录组分析

Wuweiyi Han^1,2, Xiaojuan Fei³, Fan Yang²

¹Hebei Key Laboratory of Preventive Veterinary Medicine, College of Animal Science and Technology, Hebei Normal University of Science &Technology, Qinhuangdao, 066004, China.

|January 15, 2024

概括

膀性口腔炎病毒 (VSV) 感染会改变宿主基因表达,激活像MAPK和TNF这样的免疫通路. 这项研究为了解VSV与宿主相互作用及其作为疫苗载体的使用提供了基础.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

膀性口腔炎病毒 (VSV) 是一种致动物和人类病变的狂犬病病毒.
VSV作为一个模型病毒用于分子工具,疫苗和瘤学载体.
了解VSV主机交互对于其应用程序至关重要.

研究的目的:

在VSV感染期间分析宿主基因表达变化.
识别差异表达基因 (DEG) 和长非编码RNA (lncRNA).
为VSV作为疫苗载体的应用提供理论基础.

主要方法:

用RNA测序 (RNA-Seq) 来分析BHK-21细胞中的基因表达.
基因本体学和基因和基因组 (KEGG) 路径丰富分析的京都百科全书.
定量逆转录PCR (RT-qPCR) 用于验证选定的DEGs.

主要成果:

24小时后,VSV感染改变了BHK-21细胞中的1015个mRNA和161个lncRNA.
在亡,癌症,疾病和免疫通路 (例如,TNF,P53,MAPK,NF-kappaB) 中,DEGs和lncRNAs得到了丰富.
通过RT-qPCR验证了十个选定的基因的差异表达,证实了RNA-Seq的发现.

结论:

VSV感染改变了宿主代谢网络,并激活了像MAPK和TNF这样的免疫路径.
这些发现提供了对VSV主机交互机制的见解.
这项研究支持VSV作为有效的疫苗载体的潜力.

关键词:

不同表达的基因.这是一个LncRNARNA.在RNA-Seqq.膀性口腔炎病毒的发生.它们是mRNARNA.

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