Ito Y, Nishiyama Y, Shimokata K, Maeno K
Arch Virol. 1984;80(1):33-45. doi: 10.1007/BF01315292.
A carrier culture of L cells persistently infected with Sendai virus (steady state) designated as L-Sendaits cells was established with a temperature-sensitive strain of the virus. When interferon was added to culture fluids from the start of the cultures at permissive (35 degrees C) or non-permissive temperature (38 degrees C), cell-associated infectivity was unaffected at 35 degrees C, while it was unexpectedly enhanced at 38 degrees C, although the cell-associated infectivity was titrated after further incubation at 32 degrees C for 2 days. The titer of cell-associated infectivity was increased by subculturing in the continuous presence of interferon at 38 degrees C. The effect of interferon on the paradoxical enhancement of cell-associated infectivity was shown to be dose dependent. When L-Sendaits cells were successively subcultured 6 times at 38 degrees C in the continuous presence or absence of interferon, more than 95 per cent of the cells contained a detectable amount of nucleocapsid (NP) antigen in the presence of interferon, whereas the antigen could be detected in only 30-40 per cent of the cells subcultured in the absence of interferon. Only when the cells subcultured at 38 degrees C in the presence of interferon were transferred to permissive temperature, could the distinct hemadsorbing and cell-associated hemagglutinating activities and the release of virus particles, as measured by hemagglutinating activity in the culture fluids, be detected. Cells subcultured in the presence of interferon accumulated more virus polypeptides than in the absence of interferon. Accumulation of virus specific RNA in the cells subcultured in the presence of interferon was about twice as much as that in the absence of interferon. Larger sized RNA (probably 50S) was the major species and two smaller RNAs could be detected in both the treated and untreated cells. When L-Sendaits cells were cultured at 38 degrees C in the presence of interferon, their multiplication was clearly inhibited. However, the cells which were subcultured twice at 38 degrees C in the continuous presence of interferon acquired resistance to the anti-cell proliferative action of interferon. Interestingly, the conversion of the sensitive state to resistant state of the cells was reversible.
用一种温度敏感型仙台病毒株建立了持续感染仙台病毒的L细胞载体培养物(稳定状态),命名为L-Sendaits细胞。当从培养开始就在允许温度(35℃)或非允许温度(38℃)下向培养液中添加干扰素时,在35℃时细胞相关感染性不受影响,而在38℃时却意外增强,不过细胞相关感染性是在32℃进一步孵育2天后进行滴定的。在38℃持续存在干扰素的情况下传代培养可提高细胞相关感染性的滴度。结果表明,干扰素对细胞相关感染性的反常增强作用呈剂量依赖性。当L-Sendaits细胞在有或无干扰素的情况下于38℃连续传代6次时,在有干扰素存在的情况下,超过95%的细胞含有可检测量的核衣壳(NP)抗原,而在无干扰素传代培养的细胞中,仅30%-40%的细胞能检测到该抗原。只有当在有干扰素存在的情况下于38℃传代培养的细胞转移到允许温度时,才能检测到明显的血细胞吸附和细胞相关血凝活性以及通过培养液中的血凝活性测定的病毒颗粒释放。在有干扰素存在的情况下传代培养的细胞比无干扰素时积累更多的病毒多肽。在有干扰素存在的情况下传代培养的细胞中病毒特异性RNA的积累量约为无干扰素时的两倍。较大尺寸的RNA(可能是50S)是主要种类,在处理和未处理的细胞中均可检测到两种较小的RNA。当L-Sendaits细胞在有干扰素的情况下于38℃培养时,其增殖明显受到抑制。然而,在持续存在干扰素的情况下于38℃传代培养两次的细胞获得了对干扰素抗细胞增殖作用的抗性。有趣的是,细胞从敏感状态向抗性状态的转变是可逆的。