Stampfer M, Baltimore D, Huang A S
J Virol. 1969 Aug;4(2):154-61. doi: 10.1128/JVI.4.2.154-161.1969.
Plaque-forming B particles of vesicular stomatitis virus (VSV) induce the synthesis of virus-specific ribonucleic acid (RNA) in Chinese hamster ovary cells, whereas defective T particles do not. Infection with low input multiplicities of B results in the formation of four species of RNA. During infection with high multiplicities, RNA synthesis begins with mainly these four species of RNA but gradually shifts to a new pattern of RNA synthesis involving five other species of RNA. The change can also be induced by superinfection with T at 2.5 hr after infection with a low multiplicity of B. T added at the same time as B prevents virtually all RNA synthesis. Synthesis of the first group of RNA species correlates with the formation of B particles, whereas synthesis of the second group correlates with the formation of T particles. The various species of RNA formed after infection with VSV particles include single-stranded RNA, a completely double-stranded RNA, and RNA with partially double-stranded regions. These observations begin to establish a molecular basis for understanding the ability of T particles to interfere with the growth of B particles.
水泡性口炎病毒(VSV)的噬菌斑形成B颗粒可诱导中国仓鼠卵巢细胞中病毒特异性核糖核酸(RNA)的合成,而缺陷型T颗粒则不能。以低感染复数感染B会导致四种RNA的形成。在高感染复数感染期间,RNA合成开始时主要是这四种RNA,但逐渐转变为涉及其他五种RNA的新RNA合成模式。这种变化也可在低复数感染B后2.5小时用T超感染诱导。与B同时添加T实际上会阻止所有RNA合成。第一组RNA种类的合成与B颗粒的形成相关,而第二组的合成与T颗粒的形成相关。用VSV颗粒感染后形成的各种RNA种类包括单链RNA、完全双链RNA和具有部分双链区域的RNA。这些观察结果开始为理解T颗粒干扰B颗粒生长的能力建立分子基础。