Grunwald-Beard L, Gamliel H, Parag G, Vedantham S, Zakay-Rones Z
Department of Virology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
J Cancer Res Clin Oncol. 1991;117(6):561-7. doi: 10.1007/BF01613289.
Interaction of active and UV-inactivated vaccinia virus at high multiplicity caused cytological changes and inhibition in cellular protein and DNA synthesis, thus arresting the multiplication of Burkitt-lymphoma-derived Daudi cells and eventually killing the cells. Adsorption to the cells but the lack of penetration was evident by immunofluorescence, electron microscopy and [3H]thymidine-labeled virus incorporation. Viral DNA synthesis or virus replication was not demonstrated. Thus, it appears that the massive adsorption of viral particles, active or UV-inactivated, or possibly a "toxic" component that resides in the virion, damages the plasma membrane and may be responsible for killing the cells by a mechanism of lysis from without.
活性痘苗病毒与紫外线灭活的痘苗病毒在高感染复数下相互作用，导致细胞发生细胞学变化，并抑制细胞蛋白质和DNA合成，从而阻止源自伯基特淋巴瘤的Daudi细胞增殖，最终杀死细胞。通过免疫荧光、电子显微镜和[3H]胸腺嘧啶核苷标记病毒掺入法可明显看出病毒吸附到细胞上，但未发生穿透。未检测到病毒DNA合成或病毒复制。因此，似乎大量吸附的病毒颗粒，无论是活性的还是紫外线灭活的，或者可能是病毒粒子中存在的一种“毒性”成分，都会损伤质膜，并可能通过从外部裂解的机制导致细胞死亡。
