定量蛋白质组学分析表明 p38 MAPK 途径参与了牛副流感病毒 3 型的复制。
Quantitative proteomic analysis shows involvement of the p38 MAPK pathway in bovine parainfluenza virus type 3 replication.
机构信息
Heilongjiang Bayi Agricultural University, Daqing, 163319, China.
Daqing Center of Inspection and Testing for Rural Affairs Agricultural Products and Processed Products, Ministry of Agriculture and Rural Affairs, Heilongjiang Bayi Agricultural University, Daqing, 163319, China.
出版信息
Virol J. 2022 Jul 13;19(1):116. doi: 10.1186/s12985-022-01834-x.
BACKGROUND
Bovine parainfluenza virus type 3 (BPIV3) infection often causes respiratory tissue damage and immunosuppression and further results in bovine respiratory disease complex (BRDC), one of the major diseases in dairy cattle, caused huge economical losses every year. However, the pathogenetic and immunoregulatory mechanisms involved in the process of BPIV3 infection remain unknown. However, the pathogenetic and immunoregulatory mechanisms involved in the process of BPIV3 infection remain unknown. Proteomics is a powerful tool for high-throughput identification of proteins, which has been widely used to understand how viruses interact with host cells.
METHODS
In the present study, we report a proteomic analysis to investigate the whole cellular protein alterations of MDBK cells infected with BPIV3. To investigate the infection process of BPIV3 and the immune response mechanism of MDBK cells, isobaric tags for relative and absolute quantitation analysis (iTRAQ) and Q-Exactive mass spectrometry-based proteomics were performed. The differentially expressed proteins (DEPs) involved in the BPIV3 invasion process in MDBK cells were identified, annotated, and quantitated.
RESULTS
A total of 116 proteins, which included 74 upregulated proteins and 42 downregulated proteins, were identified as DEPs between the BPIV3-infected and the mock-infected groups. These DEPs included corresponding proteins related to inflammatory response, immune response, and lipid metabolism. These results might provide some insights for understanding the pathogenesis of BPIV3. Fluorescent quantitative PCR and western blotting analysis showed results consistent with those of iTRAQ identification. Interestingly, the upregulated protein MKK3 was associated with the p38 MAPK signaling pathway.
CONCLUSIONS
The results of proteomics analysis indicated BPIV3 infection could activate the p38 MAPK pathway to promote virus replication.
背景
牛副流感病毒 3 型（BPIV3）感染常导致呼吸道组织损伤和免疫抑制，进一步导致牛呼吸道疾病复合症（BRDC），这是奶牛的主要疾病之一，每年造成巨大的经济损失。然而，BPIV3 感染过程中的发病机制和免疫调节机制尚不清楚。然而，BPIV3 感染过程中的发病机制和免疫调节机制尚不清楚。蛋白质组学是一种高通量鉴定蛋白质的强大工具，已广泛用于了解病毒如何与宿主细胞相互作用。
方法
本研究报告了一项蛋白质组学分析，以研究感染 BPIV3 的 MDBK 细胞的全细胞蛋白变化。为了研究 BPIV3 的感染过程和 MDBK 细胞的免疫反应机制，我们进行了相对和绝对定量同位素标记（iTRAQ）和 Q-Exactive 质谱基于蛋白质组学分析。鉴定、注释和定量了参与 BPIV3 入侵 MDBK 细胞过程的差异表达蛋白（DEPs）。
结果
共鉴定出 116 种蛋白质，其中包括 74 种上调蛋白和 42 种下调蛋白，这些蛋白质被鉴定为 BPIV3 感染组和 mock 感染组之间的差异表达蛋白。这些 DEPs 包括与炎症反应、免疫反应和脂质代谢相关的相应蛋白。这些结果可能为理解 BPIV3 的发病机制提供一些见解。荧光定量 PCR 和 Western blot 分析结果与 iTRAQ 鉴定结果一致。有趣的是，上调蛋白 MKK3 与 p38 MAPK 信号通路有关。
结论
蛋白质组学分析结果表明，BPIV3 感染可激活 p38 MAPK 通路，促进病毒复制。
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