Flipsen J T, Mans R M, Kleefsman A W, Knebel-Mörsdorf D, Vlak J M
Department of Virology, Agricultural University, Wageningen, The Netherlands.
J Virol. 1995 Jul;69(7):4529-32. doi: 10.1128/JVI.69.7.4529-4532.1995.
Deletion of the ecdysteroid UDP-glucosyltransferase gene (egt) from the Autographa californica nuclear polyhedrosis virus (AcNPV) genome increases the speed of killing of this virus (D. R. O'Reilly and L. K. Miller, Bio/Technology 9:1086-1089, 1991). Second-instar Spodoptera exigua larvae are killed more rapidly by the egt deletion mutant of AcNPV than by wild-type AcNPV. Unlike wild-type AcNPV-infected larvae, larvae infected with an egt deletion mutant molt and resume feeding as mock-infected larvae do. Wild-type AcNPV and egt deletion mutant recombinants marked with a lacZ gene were used to study their pathogenesis in insects. Histopathological investigation revealed that early degeneration of the Malpighian tubules, not the molting per se, may be the cause of this increased speed of killing by AcNPV.
从苜蓿银纹夜蛾核型多角体病毒(AcNPV)基因组中删除蜕皮甾体UDP-葡萄糖基转移酶基因(egt)可提高该病毒的致死速度(D. R. 奥赖利和L. K. 米勒,《生物技术》9:1086 - 1089,1991)。与野生型AcNPV相比,AcNPV的egt缺失突变体杀死二龄甜菜夜蛾幼虫的速度更快。与感染野生型AcNPV的幼虫不同,感染egt缺失突变体的幼虫会蜕皮并恢复进食,就像模拟感染的幼虫一样。用带有lacZ基因标记的野生型AcNPV和egt缺失突变体重组体来研究它们在昆虫中的发病机制。组织病理学研究表明,马氏管的早期退化,而非蜕皮本身,可能是AcNPV致死速度加快的原因。