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Ⅰ型单纯疱疹病毒(herpes simplex virus1,HSV-1)在宿主体内形成两种感染模式,不同感染模式的建立与病毒α基因的表达相关.作为病毒α基因表达产物之一的ICP22在病毒复制中发挥了多重作用,但其确切功能尚不清楚.实验利用氯霉素乙酰转移酶(chloram-phenicol acetyl transferase,CAT)报告系统发现ICP22非特异地抑制多种病毒或细胞启动子的转录启动作用,而且该抑制作用不受特定的病毒或细胞启动子上游调控元件影响.进一步的实验发现,HSV病毒蛋白VP16通过结合α4基因启动子上游特定元件解除ICP22对α4基因的转录抑制.这些结果提示,ICP22和VP16可能共同参与α基因的转录调控,从而建立HSV-1裂解性增殖或潜伏性感染.
The herpes simplex virus 1 (HSV-1) forms two kinds of infection patterns in the host body, and the establishment of different infection patterns is related to the expression of the viral α gene. ICP22, one of the viral alpha gene expression products, Play a multiple role, but its exact function is not clear.Using the chloram-phenicol acetyl transferase (CAT) reporter system found that ICP22 non-specific inhibition of a variety of viruses or cell promoter transcriptional activation, This inhibition was not affected by specific viral or cellular promoter upstream regulatory elements.Further experiments found that HSV viral protein VP16 releases the transcriptional inhibition of α4 gene by ICP22 by binding specific elements upstream of α4 gene promoter.These results suggest that ICP22 and VP16 may participate in the transcriptional regulation of α gene, thereby establishing HSV-1 lytic proliferative or latent infection.