Yura Y, Terashima K, Iga H, Kondo Y, Yanagawa T, Yoshida H, Hayashi Y, Sato M
Arch Virol. 1987;96(1-2):17-28. doi: 10.1007/BF01310987.
We have shown that a latent infection of herpes simplex virus type 2 (HSV-2) can be established in a human neuroblastoma cell line IMR-32 if the infected cells are cultured at 40 degrees C. In the present study, viral polypeptides and cellular heat-shock proteins which were synthesized in HSV-2 infected IMR-32 cells cultured at 40 degrees C were analyzed by polyacrylamide gel electrophoresis. It was found that the synthesis of late viral polypeptide ICP 5 was markedly reduced in the infected cells at 40 degrees C as compared with those at 37 degrees C. Although infection of IMR-32 cells with HSV-2 at 40 degrees C resulted in shutoff of cellular protein synthesis, it was found that some cellular heat-shock proteins (90, 72 and 70 kd polypeptides) were synthesized and accumulated intracellularly. These findings suggest that modification of cascade regulation of HSV-2 polypeptide synthesis and/or accumulation of heat-shock proteins may be involved in the incomplete arrest of virus growth and in survival of the infected cells, leading to the establishment of HSV-2 latency in IMR-32 cells.
我们已经证明，如果将感染细胞在40摄氏度下培养，单纯疱疹病毒2型（HSV - 2）可以在人神经母细胞瘤细胞系IMR - 32中建立潜伏感染。在本研究中，通过聚丙烯酰胺凝胶电泳分析了在40摄氏度下培养的HSV - 2感染的IMR - 32细胞中合成的病毒多肽和细胞热休克蛋白。结果发现，与在37摄氏度下培养的感染细胞相比，在40摄氏度下感染细胞中晚期病毒多肽ICP 5的合成明显减少。尽管在40摄氏度下用HSV - 2感染IMR - 32细胞导致细胞蛋白质合成停止，但发现一些细胞热休克蛋白（90、72和70千道尔顿多肽）在细胞内合成并积累。这些发现表明，HSV - 2多肽合成的级联调节的改变和/或热休克蛋白的积累可能与病毒生长的不完全停滞以及感染细胞的存活有关，从而导致HSV - 2在IMR - 32细胞中建立潜伏感染。
