College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Research Center for African Swine Fever Prevention and Control, South China Agricultural University, Guangzhou 510642, China.
Viruses. 2021 Jun 26;13(7):1236. doi: 10.3390/v13071236.
In 2018, African swine fever broke out in China, and the death rate after infection was close to 100%. There is no effective and safe vaccine in the world. In order to better characterize and understand the virus-host-cell interaction, quantitative proteomics was performed on porcine alveolar macrophages (PAM) infected with ASFV through tandem mass spectrometry (TMT) technology, high-performance liquid chromatography (HPLC), and mass spectrometry (MS). The proteome difference between the simulated group and the ASFV-infected group was found at 24 h. A total of 4218 proteins were identified, including 306 up-regulated differentially expressed proteins and 238 down-regulated differentially expressed proteins. Western blot analysis confirmed changes in the expression level of the selected protein. Pathway analysis is used to reveal the regulation of protein and interaction pathways after ASFV infection. Functional network and pathway analysis can provide an insight into the complexity and dynamics of virus-host cell interactions. Further study combined with proteomics data found that ARG1 has a very important effect on ASFV replication. It should be noted that the host metabolic pathway of ARG1-polyamine is important for virus replication, revealing that the virus may facilitate its own replication by regulating the level of small molecules in the host cell.
2018 年,非洲猪瘟在中国爆发,感染后的死亡率接近 100%。目前世界上没有有效和安全的疫苗。为了更好地描述和理解病毒-宿主细胞的相互作用,本研究通过串联质谱(TMT)技术、高效液相色谱(HPLC)和质谱(MS)对感染 ASFV 的猪肺泡巨噬细胞(PAM)进行了定量蛋白质组学研究。在模拟组和 ASFV 感染组之间发现了 24 小时时的蛋白质组差异。共鉴定出 4218 种蛋白质,包括 306 种上调差异表达蛋白和 238 种下调差异表达蛋白。Western blot 分析证实了所选蛋白表达水平的变化。通过通路分析揭示了 ASFV 感染后蛋白质和相互作用通路的调控。功能网络和通路分析可以深入了解病毒-宿主细胞相互作用的复杂性和动态性。进一步的研究结合蛋白质组学数据发现,ARG1 对 ASFV 的复制有非常重要的影响。值得注意的是,ARG1-多胺的宿主代谢途径对病毒复制很重要,这表明病毒可能通过调节宿主细胞中小分子的水平来促进自身的复制。