格尔德霉素抗病毒作用的相关基因研究  被引量:2

The Genes Associated with Geldanamycin Inhibiting Replication of Herpes Simplex Virus Type 1

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作  者:李怡璇[1] 刘民[1] 李欣[1] 汤华[1] 

机构地区:[1]天津医科大学基础医学院

出  处:《病毒学报》2008年第3期208-212,共5页Chinese Journal of Virology

摘  要:格尔德霉素(Geldanamycin,GA)作为一种苯醌安莎霉素类抗生素,能与热休克蛋白90特异性结合,具有广谱的抗病毒作用。为了从转录水平上研究GA抗病毒的分子机制,本研究以单纯疱疹病毒I型(Herpes simplex virus type1,HSV-1)为对象,在确定药物有效抗病毒作用的基础上,采用基因芯片技术分析了在HeLa细胞中病毒感染和药物处理对细胞表达谱的影响,并筛选出GA抗病毒作用的可能相关基因。同时用半定量RT-PCR方法对GA诱导上调、HSV-1诱导下调的基因(ACTG1、RAN、SOD1)以及GA诱导下调、HSV-1诱导上调的基因(HYAL1)进行了验证。研究GA抗病毒作用对细胞表达谱的影响,有利于深入理解药物的抗病毒机制。Geldanamycin (GA), an ansamycin antibiotic specifically binding heat shock protein 90 (Hsp90), exhibits a broad-spectrum antiviral effect. Herpes simplex virus type 1 (HSV-1) replication in vitro was significantly inhibited by GA treatment. To explore the antiviral mechanism of GA against HSV-1, the 7267-spot human long oligonucleotide microarrays were applied to investigate the genes which might involved in the antiviral activity of GA in HeLa cells infected by HSV-1. Meanwhile, the reverse regulation of GA and HSV-1 on ACTG1,RAN,SOD1,HYAL1 were validated by using semiuantitative RT-PCR. It is the first report of gene expression profile in cells infected by virus with GA treatment. The general impact of GA on cellular transcription may help to gain an insight into mechanism of its antiviral effect.

关 键 词:格尔德霉素 单纯疱疹病毒Ⅰ型 基因芯片 HELA细胞 

分 类 号:R978.7[医药卫生—药品]

 

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