Schek N, Bachenheimer S L
J Virol. 1985 Sep;55(3):601-10. doi: 10.1128/JVI.55.3.601-610.1985.
We have used Northern blot hybridization to study the accumulation of specific cellular mRNAs in Vero cells infected with herpes simplex virus (HSV) type 1 or type 2. HSV-1 infection decreased the cytoplasmic levels of beta- and gamma-actin, beta-tubulin, and histone H3 and H4 mRNAs, though not all at the same rate. HSV-2 infection resulted in a more rapid decrease in actin and histone mRNA levels compared with HSV-1 infection. The turnover rate of each type of mRNA studied was accelerated in HSV-infected cells compared with the rate in uninfected cells. Cellular mRNA degradation was induced by HSV infection under conditions of (i) inhibition of de novo protein synthesis, (ii) inhibition of de novo RNA synthesis, (iii) infection with HSV-1(17) tsK, which fails to produce early and late viral gene products at the nonpermissive temperature, and (iv) infection with purified virions in the presence of actinomycin D. We have concluded that, in Vero cells, cellular mRNA degradation is induced by a factor associated with the infecting HSV virion and thus does not require de novo RNA or protein synthesis. Despite the overall inhibition of cellular mRNA accumulation, a novel 2.2-kilobase cytoplasmic actin transcript was produced in HSV-infected cells when viral gene expression was allowed. The level of accumulation of cytoplasmic host mRNAs was compared with the rate of cellular protein synthesis under different conditions of infection. This analysis suggests that both HSV-1 and HSV-2 require an additional function(s) to completely inhibit cellular protein synthesis.
我们运用Northern印迹杂交技术，研究了1型或2型单纯疱疹病毒（HSV）感染的Vero细胞中特定细胞mRNA的积累情况。HSV - 1感染降低了β - 肌动蛋白、γ - 肌动蛋白、β - 微管蛋白以及组蛋白H3和H4 mRNA的细胞质水平，不过降低速率不尽相同。与HSV - 1感染相比，HSV - 2感染导致肌动蛋白和组蛋白mRNA水平下降得更快。与未感染细胞相比，HSV感染细胞中所研究的每种mRNA的周转率都加快了。在以下条件下，HSV感染可诱导细胞mRNA降解：（i）抑制从头蛋白质合成；（ii）抑制从头RNA合成；（iii）用HSV - 1(17)tsK感染，该病毒在非允许温度下无法产生早期和晚期病毒基因产物；（iv）在放线菌素D存在的情况下用纯化的病毒粒子感染。我们得出结论，在Vero细胞中，细胞mRNA降解是由与感染性HSV病毒粒子相关的一种因子诱导的，因此不需要从头RNA或蛋白质合成。尽管细胞mRNA积累总体受到抑制，但当允许病毒基因表达时，HSV感染的细胞中会产生一种新的2.2千碱基细胞质肌动蛋白转录本。在不同感染条件下，比较了细胞质宿主mRNA的积累水平与细胞蛋白质合成速率。该分析表明，HSV - 1和HSV - 2都需要额外的功能来完全抑制细胞蛋白质合成。
