爱泼斯坦-巴尔病毒的感染机制。I. 超感染的拉吉细胞中病毒DNA复制及非感染性病毒颗粒的形成
Mechanisms of infection with Epstein-Barr virus. I. Viral DNA replication and formation of noninfectious virus particles in superinfected Raji cells.
作者信息
Yajima Y, Nonoyama M
出版信息
J Virol. 1976 Jul;19(1):187-94. doi: 10.1128/JVI.19.1.187-194.1976.
Human lymphoblastoid Raji cells, which do not produce virus, supported replication of Epstein-Barr virus (EBV) upon superinfection. Early antigen, viral capsid antigen, and virions were produced in Raji cells superinfected with EBV. Viral DNA replicated under complete inhibition of host cell DNA synthesis to the extent that a few micrograms of EBV DNA were recovered from 107 superinfected Raji cells, corresponding to 5,000 viral genomes/cell. Homology of the synthesized viral DNA to parental EBV DNA was more than 90%. Virions produced by the Raji cells contained a 55S DNA but failed to induce early antigen, viral capsid antigen, and viral DNA synthesis after a second superinfection of Raji cells.
不产生病毒的人淋巴母细胞样Raji细胞，在受到重叠感染时能支持爱泼斯坦-巴尔病毒（EBV）的复制。早期抗原、病毒衣壳抗原和病毒粒子在被EBV重叠感染的Raji细胞中产生。病毒DNA在宿主细胞DNA合成完全被抑制的情况下进行复制，以至于从107个被重叠感染的Raji细胞中能回收几微克的EBV DNA，相当于每个细胞有5000个病毒基因组。合成的病毒DNA与亲本EBV DNA的同源性超过90%。Raji细胞产生的病毒粒子含有55S DNA，但在Raji细胞再次受到重叠感染后未能诱导早期抗原、病毒衣壳抗原和病毒DNA合成。
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