Tuffereau C, Portner A, Roux L
J Gen Virol. 1985 Nov;66 ( Pt 11):2313-8. doi: 10.1099/0022-1317-66-11-2313.
A temperature-sensitive mutant of Sendai virus with a lesion in the haemagglutinin-neuraminidase protein (HN) (ts 271) was used to study the effect of HN cell surface expression on the fate of infected BHK-21 cells. The total amount of HN was reduced in ts 271 virus-infected cells at the non-permissive temperature (38 degrees C) presumably due to degradation of the protein. At this temperature, neither HN nor a modified form of HN were found expressed at the surface of the infected cells. BHK-21 cells infected with ts 271 were nevertheless killed by the infection at 38 degrees C as well as at 30 degrees C. These results ruled out the hypothesis that the lack of HN cell surface expression could be the unique requirement allowing BHK cell survival.
利用一种在血凝素神经氨酸酶蛋白(HN)中存在损伤的仙台病毒温度敏感突变体(ts 271)来研究HN细胞表面表达对受感染的BHK-21细胞命运的影响。在非允许温度(38摄氏度)下,ts 271病毒感染的细胞中HN的总量减少,这可能是由于该蛋白的降解所致。在此温度下,未发现感染细胞表面表达HN或其修饰形式。然而,感染ts 271的BHK-21细胞在38摄氏度和30摄氏度下均因感染而死亡。这些结果排除了缺乏HN细胞表面表达可能是BHK细胞存活的唯一必要条件这一假说。