Himeda Toshiki, Ohara Yoshiro, Asakura Kunihiko, Kontani Yasuhide, Sawada Makoto
Department of Microbiology, Kanazawa Medical University, 1-1 Uchinada, Ishikawa 920-0293, Japan.
Microb Pathog. 2005 May-Jun;38(5-6):201-7. doi: 10.1016/j.micpath.2005.01.005. Epub 2005 Apr 22.
DA subgroup strains of TMEV persist in the CNS of infected mice and induce demyelination. The mechanism(s) of virus persistence and demyelination remains unknown. DA subgroup strains synthesize a 17-kDa protein, called L*, from an initiation site out-of-frame with the polyprotein. The previous study using a mutant virus, DAL*-1 (in which the L* AUG is substituted by an ACG) showed that L* has an anti-apoptotic effect in a macrophage cell line, P388D1. Therefore, we established P388D1 cells that continuatively express L*, in order to confirm its role in TMEV-induced apoptosis. The anti-apoptotic activity of L* may be important in TMEV pathogenesis.
TMEV的DA亚组毒株在受感染小鼠的中枢神经系统中持续存在并诱导脱髓鞘。病毒持续存在和脱髓鞘的机制尚不清楚。DA亚组毒株从与多蛋白读框外的起始位点合成一种17 kDa的蛋白质，称为L*。先前使用突变病毒DAL*-1（其中L的AUG被ACG取代）的研究表明，L在巨噬细胞系P388D1中具有抗凋亡作用。因此，我们建立了持续表达L的P388D1细胞，以确认其在TMEV诱导的细胞凋亡中的作用。L的抗凋亡活性可能在TMEV发病机制中起重要作用。
