College of Life Sciences, Shihezi University, Shihezi, 832003, Xinjiang, China.
Virol J. 2021 Jun 6;18(1):119. doi: 10.1186/s12985-021-01592-2.
Bovine viral diarrhea (BVD) which is caused by Bovine viral diarrhea virus (BVDV), is an acute, contagious disease. In spite of the use of vaccines and elimination projects, BVDV still causes severe economic losses to the cattle industry for the past few years. The current study presents a preliminary analysis of the pathogenic mechanisms from the perspective of protein expression levels in infected host cells at different points in time to elucidate the infection process associated with BVDV.
We used the isobaric tags for relative and absolute quantitation (iTRAQ) technology coupled with liquid chromatography-tandem mass spectrometric (LC-MS/MS) approach for a quantitative proteomics comparison of BVDV NADL-infected MDBK cells and non-infected cells. The functions of the proteins were deduced by functional annotation and their involvement in metabolic processes explored by KEGG pathway analysis to identify their interactions.
There were 357 (47.6% downregulated, 52.4% upregulated infected vs. control), 101 (52.5% downregulated, 47.5% upregulated infected vs. control), and 66 (21.2% downregulated, 78.8% upregulated infected vs. control) proteins were differentially expressed (fold change > 1.5 or < 0.67) in the BVDV NADL-infected MDBK cells at 12, 24, and 48 h after infection. GO analysis showed that the differentially expressed proteins (DEPs) are mainly involved in metabolic processes, biological regulation and localization. KEGG enrichment analysis showed that some signaling pathways that involved in the regulation of BVDV NADL-infection and host resistance are significantly (P < 0.05) enriched at different stages of the BVDV NADL-infection, such as Endocytosis signaling pathway, FoxO signaling pathway, Homologous recombination signaling pathway and Lysosome pathway.
These results revealed that the DEPs in BVDV NADL-infected MDBK cells have a wide range of regulatory effects; in addition, they provide a lot of resources for the study of host cell proteomics after BVDV infection.
牛病毒性腹泻（BVD）由牛病毒性腹泻病毒（BVDV）引起，是一种急性、传染性疾病。尽管使用了疫苗和消除项目，BVDV 仍在过去几年给牛养殖业造成了严重的经济损失。本研究从感染宿主细胞不同时间点的蛋白表达水平角度对致病机制进行了初步分析，以阐明与 BVDV 相关的感染过程。
我们使用同位素标记相对和绝对定量（iTRAQ）技术与液相色谱-串联质谱（LC-MS/MS）联用的方法，对 BVDV NADL 感染的 MDBK 细胞和未感染细胞进行了定量蛋白质组学比较。通过功能注释推导出蛋白质的功能，并通过代谢途径分析（KEGG 通路分析）探索它们在代谢过程中的作用，以确定它们的相互作用。
在感染后 12、24 和 48 小时，BVDV NADL 感染的 MDBK 细胞中分别有 357 个（47.6%下调，52.4%上调，感染与对照相比）、101 个（52.5%下调，47.5%上调，感染与对照相比）和 66 个（21.2%下调，78.8%上调，感染与对照相比）蛋白表达水平差异显著（倍数变化>1.5 或<0.67）。GO 分析表明，差异表达蛋白（DEPs）主要参与代谢过程、生物调节和定位。KEGG 富集分析表明，一些参与 BVDV NADL 感染和宿主抗性调节的信号通路在 BVDV NADL 感染的不同阶段显著富集（P<0.05），如内吞作用信号通路、FoxO 信号通路、同源重组信号通路和溶酶体途径。
这些结果表明，BVDV NADL 感染的 MDBK 细胞中的 DEPs 具有广泛的调节作用；此外，它们为研究 BVDV 感染后宿主细胞蛋白质组学提供了丰富的资源。
