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The glycosyltransferase ST3GAL2 modulates virus proliferation and the inflammation response in porcine reproductive and respiratory syndrome virus infection
Archives of Virology ( IF 2.7 ) Pub Date : 2021-07-28 , DOI: 10.1007/s00705-021-05180-1
Xiaoyang Li 1 , Yanyu Guo 1 , Yinna Song 1 , Ruiqi Sun 1 , Min Zhu 1 , Zheng Tan 1 , Umm E Swaiba 1 , Lilin Zhang 1 , Jinhai Huang 1
Affiliation  

β-galactoside α-2,3-sialyltransferase 2 (ST3GAL2) is a member of the sialyltransferase family that mediates terminal modification of glycoproteins and glycolipids. ST3GAL2 has been found to play a role in obesity, aging, and malignant diseases. In this study, we cloned porcine ST3GAL2 (pST3GAL2) from porcine alveolar macrophages (PAMs), and its role in porcine reproductive and respiratory syndrome virus (PRRSV) infection was investigated by transcriptome analysis. pST3GAL2 was found to be located in the Golgi apparatus, and it was expressed at high levels in PRRSV-infected PAMs. Overexpression of pST3GAL2 resulted in a slight increase in PRRSV proliferation, and the interaction between pST3GAL2 and GP2a of PRRSV was detected by coimmunoprecipitation and confocal microscopy. The expression of pro-inflammatory cytokines (IFN-β, IL-2, IL-6, IL-18, IL-1β and TNF-α) was significantly inhibited in pST3GAL2-overexpressing, PRRSV-infected cells and upregulated in PRRSV-infected pST3GAL2-knockout cells, while the pattern of expression of anti-inflammatory cytokines (IL-4 and IL-10) was diametrically opposite. Our results demonstrate that the regulation of pST3GAL2 plays an important role in PRRSV proliferation and functional alterations in virus-infected cells. These results contribute to our understanding of the role of β-galactoside α-2,3-sialyltransferase 2 in antiviral immunity.



中文翻译:

糖基转移酶 ST3GAL2 调节病毒增殖和猪繁殖与呼吸综合征病毒感染的炎症反应

β-半乳糖苷 α-2,3-唾液酸转移酶 2 (ST3GAL2) 是唾液酸转移酶家族的成员,可介导糖蛋白和糖脂的末端修饰。已发现 ST3GAL2 在肥胖、衰老和恶性疾病中发挥作用。在这项研究中,我们从猪肺泡巨噬细胞 (PAMs) 中克隆了猪 ST3GAL2 (pST3GAL2),并通过转录组分析研究了其在猪繁殖与呼吸综合征病毒 (PRRSV) 感染中的作用。发现 pST3GAL2 位于高尔基体中,它在 PRRSV 感染的 PAM 中高水平表达。pST3GAL2 的过表达导致 PRRSV 增殖略有增加,通过共免疫沉淀和共聚焦显微镜检测 pST3GAL2 和 PRRSV GP2a 之间的相互作用。促炎细胞因子(IFN-β、IL-2、IL-6、IL-18、IL-1β 和 TNF-α) 在 pST3GAL2 过表达、PRRSV 感染的细胞中被显着抑制,在 PRRSV 感染的 pST3GAL2 基因敲除细胞中上调,而抗炎细胞因子(IL-4 和 IL-10)的表达模式截然相反。我们的结果表明 pST3GAL2 的调节在病毒感染细胞的 PRRSV 增殖和功能改变中起重要作用。这些结果有助于我们了解 β-半乳糖苷 α-2,3-唾液酸转移酶 2 在抗病毒免疫中的作用。我们的结果表明 pST3GAL2 的调节在病毒感染细胞的 PRRSV 增殖和功能改变中起重要作用。这些结果有助于我们了解 β-半乳糖苷 α-2,3-唾液酸转移酶 2 在抗病毒免疫中的作用。我们的结果表明 pST3GAL2 的调节在病毒感染细胞的 PRRSV 增殖和功能改变中起重要作用。这些结果有助于我们了解 β-半乳糖苷 α-2,3-唾液酸转移酶 2 在抗病毒免疫中的作用。

更新日期:2021-09-07
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