Bukrinskaya A G, Klimenko S M, Smirnov Y A, Guschin B V
J Virol. 1968 Jul;2(7):752-8. doi: 10.1128/JVI.2.7.752-758.1968.
Increase of infectivity for embryonated eggs was observed in Ehrlich ascites tumor cells after intraperitoneal inoculation of Sendai virus into tumor-bearing mice. Virus-induced actinomycin-resistant ribonucleic acid consisting of 14S, 18S, 22S, 35S, and 48S was synthesized, and S antigen was produced in infected cells. The infectivity was suggested to be due to viral ribonucleoprotein for the following reasons: (i) the infectivity was unaffected by V antiserum but was abolished by whole hyperimmune serum, (ii) the infectivity was resistant to ribonuclease, (iii) virus particles were found neither in cells nor on red blood cell stroma treated with cellular extracts, (iv) structures similar to Sendai virus ribonucleoprotein with a maximal length of 10,500 A were observed in cellular extracts.
将仙台病毒腹腔接种到荷瘤小鼠体内后,在艾氏腹水瘤细胞中观察到对鸡胚的感染性增加。合成了由14S、18S、22S、35S和48S组成的病毒诱导的放线菌素抗性核糖核酸,并在感染细胞中产生了S抗原。感染性被认为是由于病毒核糖核蛋白,原因如下:(i)感染性不受V抗血清影响,但被全效超免疫血清消除;(ii)感染性对核糖核酸酶有抗性;(iii)在用细胞提取物处理的细胞或红细胞基质上均未发现病毒颗粒;(iv)在细胞提取物中观察到与仙台病毒核糖核蛋白相似的结构,最大长度为10,500埃。