牛痘病毒与脑心肌炎病毒的双重感染系统。
System of double infection between vaccinia virus and mengovirus.
作者信息
Freda C E, Buck C A
出版信息
J Virol. 1971 Sep;8(3):293-302. doi: 10.1128/JVI.8.3.293-302.1971.
When L cells are simultaneously infected with vaccinia virus and mengovirus, double interference in the replication of both viruses is observed. Superinfection of vaccinia virus-infected cells by mengovirus during the first 5 hr of infection reduces vaccinia virus yields to between 1 and 3% of controls. The yields of mengovirus are reduced to between 1 and 16% of controls, depending upon the time of superinfection. The replication of vaccinia deoxyribonucleic acid is not inhibited by mengovirus; it is only delayed. On the other hand, vaccinia multiplication severely hinders the replication of mengovirus ribonucleic acid. The double-infected system, at early times, synthesizes proteins that resemble those synthesized in the vaccinia virus-infected cells. Later in infection, however, the pattern is switched to proteins synthesized by mengovirus-infected cells. Possible mechanisms for this double interference in multiplication are discussed.
当L细胞同时感染痘苗病毒和脑心肌炎病毒时，可观察到两种病毒复制过程中的双重干扰现象。在感染的最初5小时内，脑心肌炎病毒对已感染痘苗病毒的细胞进行超感染，会使痘苗病毒的产量降至对照的1%至3%。脑心肌炎病毒的产量则降至对照的1%至16%，这取决于超感染的时间。痘苗病毒脱氧核糖核酸的复制不受脑心肌炎病毒的抑制，只是有所延迟。另一方面，痘苗病毒的增殖严重阻碍脑心肌炎病毒核糖核酸的复制。在感染早期，双重感染系统合成的蛋白质类似于在感染痘苗病毒的细胞中合成的蛋白质。然而，在感染后期，模式转变为感染脑心肌炎病毒的细胞合成的蛋白质。文中讨论了这种增殖双重干扰的可能机制。
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