流感病毒感染诱导的蛋白质合成关闭与PKR活性无关。
Protein synthesis shut-off induced by influenza virus infection is independent of PKR activity.
作者信息
Zürcher T, Marión R M, Ortín J
机构信息
Centro Nacional de Biotecnología (CSIC), Campus de Cantoblanco, 28049 Madrid, Spain.
出版信息
J Virol. 2000 Sep;74(18):8781-4. doi: 10.1128/jvi.74.18.8781-8784.2000.
Abstract
The role of PKR activity in influenza virus-induced cell shut-off was studied by infection of PKR(+) or PKR(-) cell cultures and metabolic labeling in vivo. No differences in the synthesis of viral proteins or the decay of cellular protein synthesis were observed. To investigate the relevance of the inhibition of cellular pre-mRNA polyadenylation and nucleocytoplasmic transport in virus-induced shut-off, we carried out similar experiments with mutant viruses lacking C-terminal sequences of NS1 protein. No differences in the shut-off induced by mutant versus wild-type viruses were observed, indicating that these nuclear events are not relevant for shut-off. The analysis of cytoplasmic mRNA stability indicated that the accumulation of viral mRNA during the infection correlated with the progressive decay of cellular mRNA, in both the wild type and an NS1 deletion mutant.
摘要
通过感染PKR(+)或PKR(-)细胞培养物并进行体内代谢标记，研究了PKR活性在流感病毒诱导的细胞关闭中的作用。未观察到病毒蛋白合成或细胞蛋白合成衰减的差异。为了研究细胞前体mRNA聚腺苷酸化抑制和核质转运在病毒诱导的关闭中的相关性，我们用缺乏NS1蛋白C端序列的突变病毒进行了类似实验。未观察到突变病毒与野生型病毒诱导的关闭存在差异，表明这些核事件与关闭无关。细胞质mRNA稳定性分析表明，在野生型和NS1缺失突变体感染过程中，病毒mRNA的积累与细胞mRNA的逐渐衰减相关。
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