Nishiyama Y, Ito Y, Shimokata K, Kimura Y, Nagata I
J Gen Virol. 1976 Jul;32(1):85-96. doi: 10.1099/0022-1317-32-1-85.
Infection of mouse L cells with VSV leads to the formation of polykaryocytes about 4 to 12 h p.i. When anti-VSV immune serum was added during the course of infection, progression of cell fusion was soon suppressed. Cycloheximide completely suppressed the cell fusion when the drug was added within 1 h p.i., while the cell fusion was not suppressed at all when the drug was added at and after 3 h. Early polykaryocyte formation, 'fusion from without', was observed only at a low level in cells infected at very high multiplicities. The development of cell fusion induced by VSV was found to be different in several cell types, although all these cells produced a rather high yield of virus: L and C-243-3 mouse cell lines showed a high level of polykaryocytosis (80 to 100%), BHK and RK-13 cells responded at low level, and PS and Vero cells showed no cell fusion in response to VSV infection. In PS cells, however, cell fusion occurred when VSV-infected L cells were co-cultivated. From these observations, the mechanism of cell fusion induced by VSV was discussed.
用水疱性口炎病毒(VSV)感染小鼠L细胞会在感染后约4至12小时导致多核细胞的形成。在感染过程中加入抗VSV免疫血清时,细胞融合进程很快受到抑制。如果在感染后1小时内加入环己酰亚胺,它会完全抑制细胞融合,而在感染后3小时及3小时后加入该药物时,细胞融合则完全不受抑制。早期多核细胞的形成,即“从外部融合”,仅在以非常高的复数感染的细胞中以低水平观察到。尽管所有这些细胞产生的病毒产量都相当高,但发现VSV诱导的细胞融合在几种细胞类型中的发展情况有所不同:L和C - 243 - 3小鼠细胞系表现出高水平的多核细胞增多症(80%至100%),BHK和RK - 13细胞反应水平较低,而PS和Vero细胞对VSV感染不表现出细胞融合。然而,在PS细胞中,当将感染VSV的L细胞共培养时会发生细胞融合。基于这些观察结果,对VSV诱导细胞融合的机制进行了讨论。