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目的 探讨热休克蛋白70(HSP70)过表达可能有助于汉坦病毒(HTNV)持续感染.方法 在HTNV持续性感染过程中,通过Westen blotting及RT-PCR检测大脑皮层星形胶质细胞中HSP70的表达情况,并通过免疫荧光显微技术、AnnexinV及RT-PCR检测细胞凋亡.结果 与对照组相比,感染HTNV 76-118或SEOV L99的星形胶质细胞HSP70蛋白的表达增加,且在HTNV 76-118感染后3d或SEOV L99感染后2d HSP70蛋白表达达到峰值(n=15,P＜0.01,P＜0.05);感染HTNV 76-118及SEOV L99上调星形胶质细胞HSP70基因的表达,且在HTNV76-118感染后2～5d或SEOV L99感染后2～ 4d HSP70基因表达达到峰值(n=15,P＜0.01,P＜0.05).HTNV76-118或SEOV L99感染过程中,星形胶质细胞无细胞病变效应,并且病毒复制未诱导细胞凋亡.结论 HTNV感染星形胶质细胞激活了HSP70,这种改变可能抑制细胞凋亡,促进病毒持续性感染.“,”Objective To define that heat shock protein 70 (HSP70)overpression might contributed to the persistent infection of Hantaviruses (HTNV).Methods The expression of HSP70 in cortical astrocytes was examined by Western blotting and RT-PCR during Hantavirnses persistent infection.The following apoptosis was detected by immunofluorescence microscopy,AnnexinV assays and RT-PCR assay.Results Compared to control group,the expression of HSP70 protein in astrocytes infected with HTNV 76-118 or SEOV L99 increased,peak expression of HSP70 at day 3 following HTNV 76-118 infection or at day 2 following SEOV infection (n =15,P ＜0.01,P ＜0.05),and the expression of HSP70 gene in astrocytes infected with HTNV 76-118 or SEOV L99 up-regulated,peak expression of HSP70 at day 2-5 post HTNV76-118 infection and at day 2-4 post SEOV L99 infection (n =15,P ＜ 0.01,P ＜ 0.05).In the course of HTNV76-118 or SEOV L99 infection,any cytopathic effect was not shown in astrocytes and cell apoptosis was not induced by viral replication.Conclusion HSP70 induced by Hantaviruses infection might inhibit apoptosis and contribute to the viral persistent infection.