Bukrinskaia A G, Vorkunova N K, Narmanbetova R A
Vopr Virusol. 1980 Sep-Oct(5):530-4.
The effect of remantadine on penetration of influenza virus (the WSN strain) structures into MDCK cells was studied. Autoradiography of remantadine-treated cells infected with 3H-uridine-labeled virus showed remantadine to block the penetration of the parental viral structures from the perinuclear cytoplasm into the nuclei resulting in the structures aggregating in the perinuclear cytoplasm. Biophysical analysis of the viral structures recovered from the cells and analysis of their proteins by polyacrylamide gel electrophoresis showed that in remantadine-treated cells the amount of virus nucleoids (ribonucleoproteins, RNP, surrounded by a layer of M protein) increased in the perinuclear bytoplasm while the amount of intranuclear viral plasm while the amount of intranuclear viral RNPs decreased. These data suggest that the effect of remantadine is due to blocking of the second stage of deproteinization, that is, deproteinization of viral nucleoids to viral RNPs occuring in the perinuclear cytoplasm (possibly, on nuclear membrans); remantadine did not affect penetration of viral structures into the cells or the first stage of deproteinization (formation of nucleoids from virus particles). In order to inhibit deproteinization of viral structures remantadine should be present in the process of infection and be added soon after innoculation. When added 30 min after inoculation, remantadine has no effect on the intracellular distribution of viral structures.
研究了金刚乙胺对流感病毒(WSN株)结构进入MDCK细胞的影响。用3H-尿苷标记的病毒感染经金刚乙胺处理的细胞,放射自显影显示金刚乙胺可阻止亲代病毒结构从核周细胞质进入细胞核,导致这些结构在核周细胞质中聚集。对从细胞中回收的病毒结构进行生物物理分析,并通过聚丙烯酰胺凝胶电泳分析其蛋白质,结果表明,在经金刚乙胺处理的细胞中,核周细胞质中病毒核衣壳(核糖核蛋白,RNP,被一层M蛋白包围)的数量增加,而细胞核内病毒RNP的数量减少。这些数据表明,金刚乙胺的作用是由于阻断了脱蛋白化的第二阶段,即在核周细胞质(可能在核膜上)中病毒核衣壳脱蛋白化为病毒RNP的过程;金刚乙胺不影响病毒结构进入细胞或脱蛋白化的第一阶段(从病毒颗粒形成核衣壳)。为了抑制病毒结构的脱蛋白化,金刚乙胺应在感染过程中存在,并在接种后不久添加。接种后30分钟添加金刚乙胺,对病毒结构的细胞内分布没有影响。