【摘要】 旨在探究骨髓基质抗原2(bone marrow stromal antigen 2,BST-2)对猪德尔塔冠状病毒(porcine deltacoronavirus, PDCoV)在猪小肠上皮细胞(IPEC-J2)上增殖的影响。试验通过蛋白免疫印迹(Western blot)和实时荧光定量PCR(RT-qPCR)分析PDCoV感染对BST-2表达的影响。构建BST-2真核表达载体及siRNA干扰序列，通过在IPEC-J2细胞上过表达及敲低表达BST-2基因，解析BST-2对PDCoV复制的影响。通过RT-qPCR和病毒滴度检测，分析过表达BST-2蛋白对PDCoV入侵和释放的影响。结果显示，PDCoV的感染引起内源性BST-2表达水平上调。过表达BST-2的细胞中，PDCoV病毒含量明显低于对照细胞，细胞上清中的病毒滴度也显著下降；而敲低BST-2的细胞中，PDCoV的复制显著增加。过表达BST-2蛋白未影响PDCoV吸附和进入，但显著抑制PDCoV的释放。结果表明，BST-2对PDCoV增殖有很好的抑制作用，为进一步研究BST-2蛋白的功能及PDCoV的致病机理提供了理论基础。更多还原

【Abstract】 The aim of this study was to explore the effect of bone marrow stromal antigen 2(BST-2) on the proliferation of porcine deltacoronavirus(PDCoV) in porcine intestinal epithelial cells(IPEC-J2).The experiment analyzed the effect of PDCoV infection on BST-2 expression through Western blot and real-time fluorescence quantitative PCR(RT-qPCR).A eukaryotic expression vector for BST-2 was constructed,and siRNA interference sequences were designed;these constructs were then transfected into IPEC-J2 cells.The effect of BST-2 on PDCoV replication was analyzed through overexpressing and knocking down the BST-2 gene in IPEC-J2 cells.RT-qPCR and virus titer detection were used to analyze the effect of BST-2 overexpression on PDCoV entry and release.The results showed that PDCoV infection caused an increase in endogenous BST-2 expression levels.In BST-2-overexpressing cells,the PDCoV viral RNA level was significantly lower than that in control cells gene was significantly lower than that in control cells,and the virus titer in the cell supernatant also significantly decreased;while in BST-2-knockdown cells,the replication of PDCoV significantly increased.Overexpression of BST-2 protein did not affect PDCoV adsorption and entry,but significantly inhibited the release of PDCoV.The results indicated that BST-2 is an effective inhibitor of PDCoV proliferation,providing a theoretical basis for further research on the function of BST-2 and the pathogenic mechanism of PDCoV.更多还原