Salas J, Salas M L, Viñuela E
Centro de Biología Molecular (CSIC-UAM), Facultad de Ciencias, Universidad Autónoma Canto Blanco, Madrid, Spain.
Virology. 1988 May;164(1):280-3. doi: 10.1016/0042-6822(88)90646-0.
The role of the host cell RNA polymerase II in African swine fever (ASF) virus growth has been examined using inhibitors of this enzyme. The adenosine analog 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of mRNA precursor synthesis in mammalian cells, strongly inhibits the production of infectious progeny virus in Vero cells, but does not significantly affect the synthesis of virus-specific macromolecules. On the other hand, virion assembly seems to proceed normally in the presence of DRB, as virus particles can be seen in electron micrographs with a morphology indistinguishable from that observed in the absence of the inhibitor. However, taking into account the inhibition of the infectivity caused by the drug, most of these particles must be defective. In contrast with this effect of DRB on ASF virus replication, the toxin alpha-amanitin does not inhibit the production of infectious ASF virus in Vero cells or porcine alveolar macrophages. This result indicates that the host RNA polymerase II does not transcribe viral genes and that active transcription of the cell genome is not needed for ASF virus replication.
利用这种酶的抑制剂研究了宿主细胞RNA聚合酶II在非洲猪瘟(ASF)病毒生长中的作用。腺苷类似物5,6-二氯-1-β-D-呋喃核糖基苯并咪唑(DRB)是哺乳动物细胞中mRNA前体合成的抑制剂,它强烈抑制Vero细胞中传染性子代病毒的产生,但对病毒特异性大分子的合成没有显著影响。另一方面,在DRB存在的情况下,病毒粒子组装似乎正常进行,因为在电子显微镜照片中可以看到病毒粒子,其形态与在没有抑制剂的情况下观察到的形态没有区别。然而,考虑到药物对感染性的抑制作用,这些粒子中的大多数一定是有缺陷的。与DRB对ASF病毒复制的这种作用相反,毒素α-鹅膏蕈碱并不抑制Vero细胞或猪肺泡巨噬细胞中传染性ASF病毒的产生。这一结果表明,宿主RNA聚合酶II不转录病毒基因,并且ASF病毒复制不需要细胞基因组的活跃转录。