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目的 :探讨去泛素化酶抑制剂PR-619对人类单纯疱疹病毒(herpes simplex virus,HSV)复制的影响。方法 :通过In-cell Western和Western blot技术检测病毒复制及蛋白表达,同时利用real-time PCR检测相关病毒基因的表达水平。着重考察广谱去泛素化酶抑制剂PR-619对病毒m RNA转录和病毒相关蛋白合成的作用。结果:在细胞感染体系中,PR-619可以抑制HSV极早期及晚期蛋白(ICP0、ICP4和g D)的表达,从而有效阻断病毒的复制;进一步研究发现,PR-619可以增加细胞内泛素连接蛋白含量,从而抑制细胞内泛素循环,这可能是PR-619抑制病毒复制的机制。结论:HSV的复制依赖于功能化泛素的存在,而抑制细胞去泛素化酶(DUBs)活性可以阻断细胞内正常的泛素循环,从而抑制HSV复制;该研究为寻找抗HSV治疗药物或生殖道杀微生物剂新靶点提供了新方向。
Objective: To investigate the effect of deubiquitinase inhibitor PR-619 on the replication of human herpes simplex virus (HSV). Methods: The viral replication and protein expression were detected by In-cell Western blot and Western blot. Real-time PCR was used to detect the expression of related virus genes. The effect of broad-spectrum deubiquitinase inhibitor PR-619 on viral m RNA transcription and virus-related protein synthesis was investigated. Results: PR-619 could inhibit the expression of very early and late HSV proteins (ICP0, ICP4 and gD) in cell-infected system, thus effectively blocking the replication of virus. Further studies showed that PR-619 increased the intracellular expression It is possible that PR-619 inhibits the mechanism of virus replication. Conclusion: The replication of HSV depends on the existence of functionalized ubiquitin. Inhibition of cell deubiquitinase (DUBs) activity can block the normal ubiquitin cycle in cells and inhibit the replication of HSV. In order to find an anti-HSV drug Or a new target for genital microbiocides.