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VP5 mRNA表达的动力学对于培养细胞中的病毒复制并不关键。

The kinetics of VP5 mRNA expression is not critical for viral replication in cultured cells.

作者信息

Lieu P T, Wagner E K

机构信息

Program in Animal Virology, Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697, USA.

出版信息

J Virol. 2000 Mar;74(6):2770-6. doi: 10.1128/jvi.74.6.2770-2776.2000.

Abstract

We generated recombinant viruses in which the kinetics of expression of the leaky-late VP5 mRNA was altered. We then analyzed the effect of such alterations on viral replication in cultured cells. The VP5 promoter and leader sequences from positions -36 to +20, containing the TATA box and an initiator element, were deleted and replaced with a strong early (dUTPase), an equal-strength leaky-late (VP16), or a strict-late (U(L)38) promoter. We found that recombinant viruses containing the dUTPase promoter inserted in the VP5 locus expressed VP5-encoding mRNA with early kinetics, while virus with the U(L)38 promoter inserted expressed such mRNA with strict-late kinetics. Further, in spite of differences in its functional architecture, the VP16 promoter fully substituted for the VP5 promoter. Western blot analysis demonstrated that the amounts of VP5 capsid protein produced by the recombinant viruses differed somewhat; however, on complementing C32 and noncomplementing Vero cells, such viruses replicated to titers equivalent to those of the rescued wild-type virus controls. Multistep virus growth in mouse embryo fibroblasts, rabbit skin cells, and Vero cells also demonstrated equivalent replication efficiencies for both recombinant and wild-type viruses. Further, recombinant viruses did not show any impairment in their ability to replicate on serum-starved or quiescent human lung fibroblasts. We conclude that the kinetics of the essential VP5 mRNA expression is not critical for viral replication in cultured cells.

摘要

我们构建了重组病毒,其中渗漏晚期VP5 mRNA的表达动力学发生了改变。然后我们分析了这种改变对培养细胞中病毒复制的影响。从-36到+20位的VP5启动子和前导序列,包含TATA盒和起始元件,被删除并用强早期(dUTPase)、等强度渗漏晚期(VP16)或严格晚期(U(L)38)启动子取代。我们发现,在VP5基因座插入dUTPase启动子的重组病毒以早期动力学表达编码VP5的mRNA,而插入U(L)38启动子的病毒以严格晚期动力学表达此类mRNA。此外,尽管VP16启动子在功能结构上存在差异,但它完全替代了VP5启动子。蛋白质免疫印迹分析表明,重组病毒产生的VP5衣壳蛋白量有所不同;然而,在互补的C32细胞和非互补的Vero细胞上,此类病毒的复制滴度与拯救的野生型病毒对照相当。在小鼠胚胎成纤维细胞、兔皮肤细胞和Vero细胞中的多步病毒生长也表明重组病毒和野生型病毒具有相同的复制效率。此外,重组病毒在血清饥饿或静止的人肺成纤维细胞上的复制能力没有受到任何损害。我们得出结论,必需的VP5 mRNA表达动力学对培养细胞中的病毒复制并不关键。

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