Indulen M K, Kalninya V A, Gorodkova N V, Akopova I I
A.M. Kirkhenstein Institute of Microbiology, Academy of Sciences of Latvian Soviet Socialist Republic, Riga.
Acta Virol. 1987 Nov;31(6):458-62.
All rimantadine-resistant variants of influenza virus prepared by consecutive passages in the presence of rimantadine had increased virion transcriptase activity as compared to the original strains. The increased virion transcriptase activity of rimantadine-resistant strains was unrelated to the possible role of M1 protein, since RNPs isolated from the virions of these variants also revealed higher transcriptase activity as compared to RNPs isolated from rimantadine-sensitive virus. The study of rimantadine-resistant recombinant X-4 which inherited from the resistant fowl plague virus (FPV) only the gene 7 coding for M proteins provided additional evidence for the suggestion that the increased virion transcriptase activity of rimantadine-resistant influenza virus variants is coincidental rather than directly associated with such resistance.
与原始毒株相比,在金刚烷胺存在的情况下通过连续传代制备的所有抗金刚烷胺流感病毒变体,其病毒粒子转录酶活性均有所增加。抗金刚烷胺毒株的病毒粒子转录酶活性增加与M1蛋白的可能作用无关,因为从这些变体的病毒粒子中分离出的核糖核蛋白(RNP)与从金刚烷胺敏感病毒中分离出的RNP相比,也显示出更高的转录酶活性。对仅从抗禽痘病毒(FPV)继承了编码M蛋白的基因7的抗金刚烷胺重组体X-4的研究,为以下观点提供了额外证据:抗金刚烷胺流感病毒变体的病毒粒子转录酶活性增加是巧合,而非直接与此类抗性相关。