14-3-3ε在寨卡病毒感染中的作用  

The role of 14-3-3ε in Zika virus infection

作　　者：李丽炎 刘婷 蒲洁莹[1,2,3,4] 黄曦 LI Li-yan;LIU Ting;PU Jie-ying;HUANG Xi(Department of Immunology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou , Guangdong 510080;The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong 519000;Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080;Key Laboratory of Tropical Diseases Control, Sun Yat-sen University, Ministry of Education, Guangzhou, Guangdong 510080, China)

机构地区：[1]中山大学中山医学院免疫学教研室,广东广州510080 [2]中山大学附属第五人民医院,广东珠海519000 [3]中山大学人类病毒学研究所,广东广州510080 [4]中山大学热带病防治研究教育部重点实验室,广东广州510080

出　　处：《热带医学杂志》2018年第6期699-702,共4页Journal of Tropical Medicine

基　　金：国家自然科学基金(31470877;31370868;81261160323)

摘　　要：目的探讨14-3-3ε在寨卡病毒(ZIKV)感染中的作用。方法 ZIKV感染A549细胞后,Western blot方法检测14-3-3ε的表达。在A549细胞中过表达和沉默14-3-3ε,探针法和Western blot分别检测ZIKV RNA复制水平和蛋白表达水平,荧光定量PCR检测炎性因子白细胞介素-6(IL-6)和肿瘤坏死因子(TNF-α)的表达变化。采用Western blot方法检测p-P38和p-ERK信号通路在ZIKV感染后不同时间点的激活情况。结果 ZIKV感染会抑制14-3-3ε的表达,在A549细胞中,转染14-3-3ε过表达质粒后检测到ZIKV复制显著下降(P<0.05),沉默14-3-3ε后检测到ZIKV的复制显著升高(P<0.05);过表达14-3-3ε后激活p-P38和p-ERK的表达,促进炎性因子IL-6和TNF-α的表达(P<0.05)。结论ZIKV感染诱导14-3-ε表达降低,14-3-3ε能够抑制ZIKV的复制,其机制可能是通过激活p-P38和p-ERK通路来促进炎性因子IL-6和TNF-α的表达升高,进而发挥抗病毒的作用,14-3-3ε有望成为抗ZIKV的一个药物靶点。Objective To study the role of 14-3-3ε in Zika virus（ZIKV）infection.Methods Western blot method wasused to detect the expression of 14-3-3ε in ZIKV infected A549 cells.Overexpression and silencing of 14-3-3ε in A549 cells,were detected by northen blot method and Western blot,respectively.The expression of inflammatory cytokinesinterleukin-6（IL-6）and tumor necrosis factor-α（TNF-α） were detected by fluorescence quantitative PCR.The activation of p-P38 and p-ERK signaling pathways at different time points after ZIKV infection was detected by Western blot method.Results ZIKV infection inhibits the expression of 14-3-3ε.After transfection of 14-3-3ε overexpression plasmid into A549 cells,the replication of ZIKV was significantly decreased（P〈0.05）,and the replication of ZIKV was significantlyincreased after the silencing of 14-3-3ε（P0.05）.The expression of p-P38 and p-ERK was activated after 14-3-3εoverexpression.In addition,14-3-3ε promoted the expression of inflammatory cytokines IL-6 and TNF-α（P〈0.05）.Conclusion ZIKV infection lower the 14-3-3ε expression;14-3-3ε might block ZIKV replication through the activation ofp-P38 and p-ERK signaling,and promoted the inflammatory cytokines IL-6 and TNF-α expression.In sum,14-3-3ε playedan antiviral role,and was expected to be a drug target for anti-ZIKV.

关 键 词：14-3-3ε 寨卡病毒 P-ERK P-P38 

分 类 号：R373[医药卫生—病原生物学]