Langeland N, Moore L J, Holmsen H, Haarr L
Department of Biochemistry, University of Bergen, Norway.
Biochem J. 1989 Jul 15;261(2):683-6. doi: 10.1042/bj2610683.
Herpes simplex virus type 1 (HSV-1) induces altered phosphoinositide metabolism in baby hamster kidney (BHK) cells, measured as incorporation of [3H]inositol or [32P]Pi [Langeland, Haarr & Holmsen (1986) Biochem. J. 237, 707-712]. We now report that this response in the inositol phospholipids is dependent on virus-specific proteins synthesized in the beta (early) stage of virus protein synthesis. This was demonstrated both by resistance to the inhibitory effect of cycloheximide after this stage of infection, and by the use of temperature-sensitive (ts) mutants of HSV-1; ts mutants in which protein synthesis was blocked so that only the alpha proteins were expressed showed a PIP2/PIP (phosphatidylinositol 4,5-bisphosphate/phosphatidylinositol 4-monophosphate) ratio similar to uninfected cells, while ts mutants which were defective in protein synthesis at a late beta stage or later showed increased PIP2/PIP ratios similar to cells infected by wild type HSV-1.
1型单纯疱疹病毒(HSV-1)可诱导幼仓鼠肾(BHK)细胞中磷酸肌醇代谢发生改变,这可通过[3H]肌醇或[32P]Pi的掺入量来衡量[兰格兰德、哈尔及霍尔姆森(1986年),《生物化学杂志》237卷,707 - 712页]。我们现在报告,肌醇磷脂的这种反应取决于在病毒蛋白质合成的β(早期)阶段合成的病毒特异性蛋白质。这一点在感染此阶段后对放线菌酮抑制作用的抗性以及使用HSV-1的温度敏感(ts)突变体中均得到了证实;蛋白质合成受阻从而仅表达α蛋白的ts突变体显示出与未感染细胞相似的磷脂酰肌醇4,5-二磷酸/磷脂酰肌醇4-单磷酸(PIP2/PIP)比率,而在β晚期或更晚阶段蛋白质合成有缺陷的ts突变体则显示出与野生型HSV-1感染细胞相似的升高的PIP2/PIP比率。