Igarashi A
Arch Virol. 1979;62(4):303-12. doi: 10.1007/BF01318104.
When A. albopictus, clone C6/36, cells were infected with chikungunya (CHIK) virus, high virus yield accompanied by a cytopathic effect in the acute stage of infection was followed by a relatively low yield of virus over a long period of time. Virus produced from persistently infected cultures became gradually of smaller plaque size and more temperature-sensitive; however, such virus still retained pathogenicity for suckling mice even after one year of infection. When the persistently infected cells were subcultured, a dissociation was observed between the time course of cell growth and that of virus production, suggesting some intracellular mechanisms that turn off virus production. The greater part of the interference against CHIK virus by the culture medium of the persistently infected cells appeared to be mediated by the infective virus in the medium. The infective virus was easily removed from the persistently infected cells either by subculture or by cloning in the presence of anti-CHIK serum, yielding cured cultures or virus-negative clones.
当白纹伊蚊C6/36克隆细胞被基孔肯雅病毒(CHIK)感染时,在感染急性期伴随着细胞病变效应会产生高病毒产量,随后在很长一段时间内病毒产量相对较低。持续感染培养物产生的病毒斑块大小逐渐变小,对温度更敏感;然而,即使在感染一年后,这种病毒对乳鼠仍具有致病性。当对持续感染的细胞进行传代培养时,观察到细胞生长的时间进程与病毒产生的时间进程之间存在分离,这表明存在一些关闭病毒产生的细胞内机制。持续感染细胞的培养基对CHIK病毒的大部分干扰似乎是由培养基中的感染性病毒介导的。通过传代培养或在抗CHIK血清存在下进行克隆,可轻松从持续感染的细胞中去除感染性病毒,从而获得治愈的培养物或病毒阴性克隆。