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托戈托病毒和多里病毒的复制被细胞聚合酶II活性抑制剂阻断,但不会导致宿主细胞蛋白质合成的关闭。

Thogoto and Dhori virus replication is blocked by inhibitors of cellular polymerase II activity but does not cause shutoff of host cell protein synthesis.

作者信息

Siebler J, Haller O, Kochs G

机构信息

Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Federal Republic of Germany.

出版信息

Arch Virol. 1996;141(8):1587-94. doi: 10.1007/BF01718257.

Abstract

Tick-transmitted Thogoto and Dhori viruses share structural and genetic properties with the influenza viruses. Here, we compare different steps of their replication cycle in mammalian cells in comparison with influenza A virus. Viral antigens of both viruses accumulated in the nuclei of infected cells, suggesting a nuclear phase of viral replication. Furthermore, as observed with influenza viruses, transcription of Thogoto and Dhori viruses was inhibited by alpha-amanitin and actinomycin D, suggesting a dependence of viral transcription on cellular RNA polymerase II activity. In contrast to influenza viruses, Thogoto and Dhori virus infection did not lead to down-regulation of cellular protein synthesis indicating marked differences regarding the fate of infected cells.

摘要

蜱传托高托病毒和多里病毒与流感病毒具有结构和遗传特性。在此,我们将它们在哺乳动物细胞中的复制周期的不同步骤与甲型流感病毒进行比较。两种病毒的病毒抗原都在受感染细胞的细胞核中积累,表明病毒复制存在核阶段。此外,正如在流感病毒中观察到的那样,托高托病毒和多里病毒的转录受到α-鹅膏蕈碱和放线菌素D的抑制,表明病毒转录依赖于细胞RNA聚合酶II的活性。与流感病毒不同,托高托病毒和多里病毒感染不会导致细胞蛋白质合成的下调,这表明在受感染细胞的命运方面存在显著差异。

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