Leblond-Larouche L, Morais R, Zollinger M
J Gen Virol. 1979 Aug;44(2):323-31. doi: 10.1099/0022-1317-44-2-323.
A function for mitochondria in the reproduction of Rous sarcoma virus (RSV) in chronically and newly infected chick embryo cells was studied by using chloramphenicol and ethidium bromide. Chloramphenicol (CAM) and ethidium bromide (EB) were both shown to decrease the rate of growth of infected chick embryo cells and to inhibit the synthesis of mitochondrial macromolecules. Both drugs however had little or no effect on the incorporation of labelled leucine, thymidine and uridine into total cellular macromolecules. Neither CAM (80 microgram/ml) nor EB (0.4 microgram/ml) inhibited the production of infectious virus. In contrast, camptothecin, an inhibitor of cellular but not mitochondrial macromolecular synthesis, was shown to depress the production of infectious virus. The results indicate that the mitochondrial macromolecular synthesis machinery of RSV-infected chick embryo cells does not contribute to virus production.
通过使用氯霉素和溴化乙锭,研究了线粒体在慢性和新感染的鸡胚细胞中劳斯肉瘤病毒(RSV)繁殖过程中的作用。已证明氯霉素(CAM)和溴化乙锭(EB)均可降低感染的鸡胚细胞的生长速率,并抑制线粒体大分子的合成。然而,这两种药物对标记的亮氨酸、胸腺嘧啶核苷和尿苷掺入总细胞大分子的过程几乎没有影响。无论是80微克/毫升的CAM还是0.4微克/毫升的EB均未抑制传染性病毒的产生。相比之下,喜树碱是一种细胞而非线粒体大分子合成的抑制剂,已证明它可抑制传染性病毒的产生。结果表明,RSV感染的鸡胚细胞的线粒体大分子合成机制对病毒产生没有贡献。