Volkman L, Storm K, Aivazachvili V, Oppenheimer D
Department of Plant and Microbial Biology, University of California, Berkeley 94720, USA.
Virology. 1996 Nov 15;225(2):369-76. doi: 10.1006/viro.1996.0611.
Autographa californica M nuclear polyhedrosis virus (AcMNPV) terminates host protein synthesis during the late stage of infection, at approximately 14 hr postinfection (hpi). If infection takes place in the presence of cytochalasin D (CD), however, host actin synthesis is transiently stimulated and continues to be synthesized until approximately 30 hpi, and the hyperexpression of polyhedrin is delayed from about 20 hpi until about 36 hpi (S. N. Talhouk and L. E. Volkman, Virology 182, 626-634, 1991; N. Wei and L. E. Volkman, Virology 191, 42-48, 1992). To investigate whether these events are causally related, i.e., whether actin synthesis negatively affects polyhedrin synthesis, we constructed recombinant viruses that expressed actin at various levels during infection. We found that the expression of actin by a strong promoter interfered with polyhedrin synthesis at a posttranscriptional level. It also interfered with polyhedra formation, which may suggest a mechanism for the observed paucity of polyhedra in infected midgut columnar epithelial cells in vivo.
苜蓿银纹夜蛾核型多角体病毒（AcMNPV）在感染后期，即感染后约14小时，终止宿主蛋白合成。然而，如果在细胞松弛素D（CD）存在的情况下发生感染，宿主肌动蛋白合成会被短暂刺激，并持续合成至约30小时，多角体蛋白的过度表达从约20小时延迟至约36小时（S. N. 塔尔胡克和L. E. 沃尔克曼，《病毒学》182卷，626 - 634页，1991年；N. 魏和L. E. 沃尔克曼，《病毒学》191卷，42 - 48页，1992年）。为了研究这些事件是否存在因果关系，即肌动蛋白合成是否对多角体蛋白合成产生负面影响，我们构建了在感染期间表达不同水平肌动蛋白的重组病毒。我们发现，强启动子驱动的肌动蛋白表达在转录后水平干扰了多角体蛋白合成。它还干扰了多角体的形成，这可能提示了在体内感染的中肠柱状上皮细胞中观察到的多角体数量稀少的一种机制。
