Volkman L E
Department of Entomology, University of California, Berkeley 94720.
Virology. 1988 Apr;163(2):547-53. doi: 10.1016/0042-6822(88)90295-4.
Autographa californica nuclear polyhedrosis virus (AcMNPV) is a large, double-stranded DNA virus of lepidopteran insects. It replicates in the nucleus of host cells and produces two different infectious forms. One of them buds from the plasma membrane and is responsible for systemic infection in insects and for the spread of infection in cell culture. Earlier we reported that cytochalasin D (CD) inhibited the production of this form of the virus in infected IPLB-SF-21 cells by a mechanism other than the prevention of budding [L. E. Volkman, P. A. Goldsmith, and R. T. Hess (1987). Virology 156, 32-39]. Herein we present evidence that CD interferes with proper nucleocapsid assembly which indicates that microfilaments are involved in this nuclear process. The observation that phalloidin localizes in the nuclei of 24-hr infected cells in the absence, but not in the presence, of CD supports this hypothesis. Viral DNA replication and synthesis of the major capsid antigen and its transport to the nucleus are not inhibited by CD.
苜蓿银纹夜蛾核型多角体病毒（AcMNPV）是一种大型双链DNA病毒，可感染鳞翅目昆虫。它在宿主细胞的细胞核中复制，并产生两种不同的感染形式。其中一种从细胞膜出芽，负责在昆虫体内的系统性感染以及在细胞培养中的感染传播。此前我们报道，细胞松弛素D（CD）通过一种不同于阻止出芽的机制抑制了这种病毒在感染的IPLB-SF-21细胞中的产生[L.E.沃尔克曼、P.A.戈德史密斯和R.T.赫斯（1987年）。《病毒学》156，32-39]。在此我们提供证据表明，CD干扰了核衣壳的正确组装，这表明微丝参与了这一核过程。在不存在CD但存在鬼笔环肽的情况下，鬼笔环肽定位于感染24小时细胞的细胞核中的观察结果支持了这一假设。病毒DNA复制、主要衣壳抗原的合成及其向细胞核的转运不受CD的抑制。
