Koyama A Hajime, Irie Hiroshi, Kato Atsushi, Nagai Yoshiyuki, Adachi Akio
Department of Virology, The University of Tokushima Graduate School of Medicine, Tokushima 770-8503, Japan.
Microbes Infect. 2003 Apr;5(5):373-8. doi: 10.1016/s1286-4579(03)00043-1.
Sendai virus (SeV) P gene encodes a nested set of carboxyl-coterminal proteins (C', C, Y1 and Y2), which are referred to collectively as the C proteins. Characterization of the virus multiplication and cellular responses in HEp-2 cells infected with the recombinant SeV which lacks two (C' and C), three (C', C and Y1) or all the four C proteins revealed that all the recombinant viruses can grow in the cells to various extents, depending, apparently, on the number of species expressing C protein. In reverse proportion to the viral growth ability, these viruses induced apoptosis in the infected cells. These results indicate that Y2 protein has an antiapoptotic activity, and suggest that this activity works in an additive manner with the longer C protein(s) (C' and/or C) of SeV in order to suppress virus-induced apoptosis in the SeV-infected cells. Apparently, the antiapoptotic activity of the C proteins supports virus multiplication in the infected cells.
仙台病毒(SeV)的P基因编码一组羧基末端嵌套的蛋白质(C'、C、Y1和Y2),这些蛋白质统称为C蛋白。对感染了缺失两种(C'和C)、三种(C'、C和Y1)或全部四种C蛋白的重组SeV的人喉表皮样癌细胞(HEp-2细胞)中的病毒增殖和细胞反应进行表征后发现,所有重组病毒都能在细胞中不同程度地生长,这显然取决于表达C蛋白的种类数量。与病毒生长能力成反比,这些病毒在感染的细胞中诱导凋亡。这些结果表明Y2蛋白具有抗凋亡活性,并表明这种活性与SeV较长的C蛋白(C'和/或C)以累加方式起作用,以抑制SeV感染细胞中病毒诱导的凋亡。显然,C蛋白的抗凋亡活性支持病毒在感染细胞中的增殖。