Levitan D B, Blough H A
J Virol. 1976 Jun;18(3):1081-7. doi: 10.1128/JVI.18.3.1081-1087.1976.
Cell-free extracts prepared from herpes simplex virus-infected BHK-21 cells rapidly induced exogenous fusion when incubated with indicator monolayers of uninfected BHK-21 cells. Fusion was first observed at 1 h, and peak activity was reached by 4 h. Divalent cations were required for activity. Inhibition of indicator cell macromolecular synthesis, with metabolic inhibitors, failed to prevent formation of cell-free extract-induced polykaryocytes. Removal of virus particles from the cell-free extract by velocity sedimentation centrifugation did not affect cell-free extract exogenous fusion activity. Studies using molecular probes, namely, glycosidases, lectins, and antiserum (directed against either HSV envelope or capsid proteins), suggest that the factor(s) responsible for herpesvirus fusion is a fucosylated glycoprotein that is not a structural component of the virion.
从单纯疱疹病毒感染的BHK - 21细胞制备的无细胞提取物,与未感染的BHK - 21细胞指示单层一起孵育时,能迅速诱导外源性融合。融合在1小时时首次观察到,4小时时达到活性峰值。活性需要二价阳离子。用代谢抑制剂抑制指示细胞的大分子合成,未能阻止无细胞提取物诱导的多核细胞形成。通过速度沉降离心从无细胞提取物中去除病毒颗粒,不影响无细胞提取物的外源性融合活性。使用分子探针(即糖苷酶、凝集素和抗血清(针对HSV包膜或衣壳蛋白))的研究表明,负责疱疹病毒融合的因子是一种岩藻糖基化糖蛋白,它不是病毒体的结构成分。