Shiroki K, Kato H, Koike S, Odaka T, Nomoto A
Department of Microbiology, University of Tokyo, Japan.
J Virol. 1993 Jul;67(7):3989-96. doi: 10.1128/JVI.67.7.3989-3996.1993.
Two cell lines, TgSVA and TgSVB, were established from the kidneys of transgenic mice carrying the human gene encoding poliovirus receptor. The cells were highly susceptible to poliovirus infection, and a large amount of infectious particles was produced in the infected cells at 37 degrees C. However, the virus yield was greatly reduced at 40 degrees C. This phenomenon was common to all mouse cells tested. To identify the temperature-sensitive step(s) of the virus infection cycle, different steps of the infection cycle were examined for temperature sensitivity. The results strongly suggested that the growth restriction observed at 40 degrees C was due to reduced efficiency of the initiation process of virus-specific RNA synthesis. Furthermore, this restriction appeared to occur only on the synthesis of positive-strand RNA. Virus-specific RNA synthesis in crude replication complexes was not affected by the nonpermissive temperature of 40 degrees C. In vitro uridylylation of VPg seemed to be temperature sensitive only after prolonged incubation at 40 degrees C. These results indicate that a specific host factor(s) is involved in the efficient initiation process of positive-strand RNA synthesis of poliovirus and that the host factor(s) is temperature sensitive in TgSVA and TgSVB cells.
从携带编码脊髓灰质炎病毒受体的人类基因的转基因小鼠肾脏中建立了两种细胞系，TgSVA和TgSVB。这些细胞对脊髓灰质炎病毒感染高度敏感，在37℃下感染细胞中产生大量感染性颗粒。然而，在40℃时病毒产量大大降低。这种现象在所有测试的小鼠细胞中都很常见。为了确定病毒感染周期中温度敏感的步骤，对感染周期的不同步骤进行了温度敏感性检查。结果强烈表明，在40℃观察到的生长限制是由于病毒特异性RNA合成起始过程的效率降低。此外，这种限制似乎仅发生在正链RNA的合成上。粗复制复合物中的病毒特异性RNA合成不受40℃非允许温度的影响。VPg的体外尿苷酸化似乎仅在40℃长时间孵育后才对温度敏感。这些结果表明，一种特定的宿主因子参与了脊髓灰质炎病毒正链RNA合成的有效起始过程，并且该宿主因子在TgSVA和TgSVB细胞中对温度敏感。
