Transcriptome analysis of PK-15 cells expressing CSFV NS4A.

Transcriptome analysis of PK-15 cells expressing CSFV NS4A.
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表达 CSFV NS4A 的 PK-15 细胞的转录组分析

DOI:
10.1186/s12917-022-03533-9
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发表时间:
2022-12-12
影响因子:
2.6
通讯作者:
Dong, Wang
Dong, Wang
中科院分区:
农林科学2区
文献类型:
--
作者:
Lv, Huifang;Peng, Zhifeng;Jia, Bingxin;Jing, Huiyuan;Cao, Sufang;Xu, Zhikun;Dong, Wang

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猪瘟(CSF)是由猪瘟病毒(CSFV)引起的一种严重的猪病,在世界范围内造成巨大的经济损失。猪瘟病毒非结构蛋白4a (NS4A)在感染性猪瘟病毒颗粒形成中起着至关重要的作用。然而,NS4A在猪瘟感染中的功能尚不清楚。在本研究中,我们利用RNA-seq技术研究CSFV NS4A在PK-15细胞中的功能作用。与表达空载体(NC)的细胞相比,在表达NS4A的PK-15细胞中共鉴定出3893个差异表达基因(DEGs)。选择12个deg,并通过RT-qPCR进一步验证。GO和KEGG富集分析显示,这些deg与多种生物学功能相关,包括细胞粘附、细胞凋亡、宿主防御反应、炎症反应、免疫反应和自噬。有趣的是,一些与宿主免疫防御和炎症反应相关的基因被下调,一些与宿主凋亡和自噬相关的基因被上调。CSFV NS4A抑制先天免疫反应,抑制与病毒防御反应和炎症反应相关的重要基因表达,调控细胞粘附、凋亡和自噬。在线版本包含补充材料,可在10.1186/s12917-022-03533-9获得。
Classical swine fever (CSF) is a severe disease of pigs that results in huge economic losses worldwide and is caused by classical swine fever virus (CSFV). CSFV nonstructural protein 4 A (NS4A) plays a crucial role in infectious CSFV particle formation. However, the function of NS4A during CSFV infection is not well understood.  In this study, we used RNA-seq to investigate the functional role of CSFV NS4A in PK-15 cells. A total of 3893 differentially expressed genes (DEGs) were identified in PK-15 cells expressing NS4A compared to cells expressing the empty vector (NC). Twelve DEGs were selected and further verified by RT‒qPCR. GO and KEGG enrichment analyses revealed that these DEGs were associated with multiple biological functions, including cell adhesion, apoptosis, host defence response, the inflammatory response, the immune response, and autophagy. Interestingly, some genes associated with host immune defence and inflammatory response were downregulated, and some genes associated with host apoptosis and autophagy were upregulated. CSFV NS4A inhibits the innate immune response, and suppresses the expression of important genes associated with defence response to viruses and inflammatory response, and regulates cell adhesion, apoptosis and autophagy. The online version contains supplementary material available at 10.1186/s12917-022-03533-9.
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