Koyama A Hajime, Irie Hiroshi, Ueno Fumiko, Ogawa Motomi, Nomoto Akio, Adachi Akio
Department of Virology1 and Department of Ophthalmology3, School of Medicine, The University of Tokushima, Tokushima 770-8503, Japan.
Department of Pathology, Teikyo University School of Medicine, Kaga, Itabashi-ku, Tokyo 173-8650, Japan2.
J Gen Virol. 2001 Dec;82(Pt 12):2965-2972. doi: 10.1099/0022-1317-82-12-2965.
To determine an antiapoptotic activity of poliovirus type 1 (PV-1), we examined the effect of PV-1 infection on apoptosis that was induced in HEp-2 cells by the treatment with 1 M sorbitol. The virus did not induce apoptosis in the infected cells and could suppress both the fragmentation of chromosomal DNA and morphological cell and cell nuclei changes in the sorbitol-treated cells, indicating that PV-1 induces an antiapoptotic state. Comparison of the kinetics showed that this ability of the virus appeared in the infected cells at the time of progeny virus formation (maturation step of virus multiplication). Simultaneously with this antiapoptotic activity, PV-1 infection also suppressed non-apoptotic cell death induced by sodium chloride. Electron microscopic observation revealed that the cells killed by the sodium chloride treatment had undergone liquefactive necrosis, indicating that PV-1 can inhibit both apoptosis and necrosis. In addition, PV-1 can grow in the apoptotic cells, although the virus yield was reduced to a quarter of the yield in normal cells.
为了确定1型脊髓灰质炎病毒（PV-1）的抗凋亡活性，我们检测了PV-1感染对经1 M山梨醇处理诱导的HEp-2细胞凋亡的影响。该病毒在感染细胞中未诱导凋亡，并且能够抑制山梨醇处理细胞中染色体DNA的片段化以及细胞和细胞核的形态变化，表明PV-1诱导了一种抗凋亡状态。动力学比较显示，病毒的这种能力在子代病毒形成时（病毒增殖的成熟步骤）出现在感染细胞中。与这种抗凋亡活性同时，PV-1感染还抑制了由氯化钠诱导的非凋亡性细胞死亡。电子显微镜观察显示，经氯化钠处理杀死的细胞发生了液化性坏死，表明PV-1可以抑制凋亡和坏死。此外，PV-1可以在凋亡细胞中生长，尽管病毒产量降至正常细胞产量的四分之一。
