Ash R J
Virology. 1986 Dec;155(2):584-92. doi: 10.1016/0042-6822(86)90218-7.
The synthesis of herpes simplex virus (HSV) in mouse neuroblastoma cells (NB, clone 41A3) is restricted. There was a disappearance of infectious virus upon serial passage of infected cells. NB cells treated with sodium-n-butyrate for 24 hr before infection synthesized 200-2000 times more HSV than untreated cells. Infectious center assays demonstrated that the number of cells capable of producing HSV was increased as a result of butyrate pretreatment. Although host protein synthesis was inhibited by HSV infection, viral-induced protein and DNA syntheses were not detected in the absence of butyrate. Cycloheximide blocked the induction of permissiveness by butyrate suggesting that a protein(s) was responsible for allowing HSV synthesis in NB cells. Regulatable host factors involved in HSV replication in neural cells can be studied in the system described.
单纯疱疹病毒(HSV)在小鼠神经母细胞瘤细胞(NB,克隆41A3)中的合成受到限制。感染细胞连续传代后,感染性病毒消失。感染前用正丁酸钠处理NB细胞24小时,其合成的HSV比未处理的细胞多200 - 2000倍。感染中心试验表明,丁酸盐预处理使能够产生HSV的细胞数量增加。尽管HSV感染会抑制宿主蛋白合成,但在没有丁酸盐的情况下未检测到病毒诱导的蛋白和DNA合成。环己酰亚胺阻断了丁酸盐对允许性的诱导,这表明一种蛋白质负责使HSV在NB细胞中合成。在所述系统中可以研究参与神经细胞中HSV复制的可调节宿主因子。