戊型肝炎病毒感染激活补体系统

Hepatitis E Virus Infection Activates the Complement System

为了探究补体系统与戊型肝炎病毒复制的相关性,分别在HEV感染的A549细胞和BALB/c小鼠中检测C3aR、CD55和CD59蛋白的表达。利用RT-qPCR定量检测细胞和组织中补体的表达,采用免疫组化法检测HEV感染BALB/c小鼠中补体CD59及C5b-9的表达,ELISA检测补体相关炎症因子的变化。HEV感染可以激活补体蛋白C3aR、C5b-9、CD55和CD59的表达,引起补体蛋白相关炎症因子IL-10表达水平下降,IL-12和TNF-α的表达水平的上升,从而导致机体的炎症反应,加剧组织损伤。HEV感染激活补体系统并参与早期的抗病毒反应,HEV感染对补体的持续激活导致炎症因子过度表达,加重机体损伤。

To explore the correlation between complement proteins C3 aR,CD55,and CD59 and hepatitis E virus infection using A549 cells and BALB/c mice. Expression of complement genes in cells or tissues was quantified by RT-qPCR. Detection of HEV ORF2,CD59,and C5 b-9 in BALB/c mice was performed using immunohistochemistry(IHC)and immunofluorescence assay(IFA). Complement-related inflammatory factors were determined by ELISA.HEV infection activates the expression of complement proteins C3 aR,CD55,and CD59. Complement regulatory proteins CD55 and CD59 exert their inhibitory effects to promote persistent complement activation. Complement protein-related cytokines,including IL-10,were decreased following HEV infection,while IL-12 and TNF-α were increased,which may aggravate damage.HEV infection activates the complement system and participates in the early antiviral responses of the host immune system. The continuous activation of complement by HEV may lead to overexpression of complement,which may exacerbate damages.