Miyamura T, Kitahara T
Arch Virol. 1975;48(2):147-56. doi: 10.1007/BF01318147.
As early as 3--4 hours after infection with SV40 at a high input multiplicity, African green monkey (Cercopithecus aethiops) kidney (AGMK) cells developed cytoplasmic vacuolization. At 10--20 hours after infection, the vacuolization reached its maximal level, then disappeared and SV40 specific cytopathic change followed. This vacuolization developed before the synthesis of the specific T and V antigens. This early cytoplasmic vacuolization (ECV) was prevented by preincubating the virus with specific antiserum, or by heating the virus with MgCl2. The ECV could be induced by UV-irradiated SV40. Addition of metabolic inhibitors had no effect on the induction of the ECV. These results suggest that the capacity to induce the ECV resides in a structural component(s) of SV40 virion and the vacuolization is not associated with the replication of SV40.
早在以高感染复数感染SV40后3 - 4小时，非洲绿猴（长尾猴）肾（AGMK）细胞就出现了细胞质空泡化。感染后10 - 20小时，空泡化达到最高水平，然后消失，接着出现SV40特异性细胞病变变化。这种空泡化在特异性T和V抗原合成之前就已出现。通过用特异性抗血清预孵育病毒，或用MgCl2加热病毒，可防止这种早期细胞质空泡化（ECV）。UV照射的SV40可诱导ECV。添加代谢抑制剂对ECV的诱导没有影响。这些结果表明，诱导ECV的能力存在于SV40病毒粒子的一种结构成分中，且空泡化与SV40的复制无关。
