Talhouk S N, Volkman L E
Department of Entomology, University of California, Berkeley 94720.
Virology. 1991 Jun;182(2):626-34. doi: 10.1016/0042-6822(91)90603-9.
During infection by the baculovirus Autographa californica multiple nuclear polyhedrosis virus (AcMNPV), synthesis of host proteins in IPLB-Sf-21 cells is inhibited. We report here that cytochalasin D (CD), a drug that specifically interacts with actin, behaved as an antagonist in the virus-mediated shutdown of host proteins actin and tubulin. In uninfected cells, CD caused an increase in actin synthesis but had no apparent effect on tubulin synthesis. In infected cells, CD similarly enhanced actin synthesis early in infection and delayed the virus shutoff of actin synthesis by 14 hr. The shutoff of tubulin synthesis was delayed by 8 hr. Addition of CD to infected cells after host protein synthesis ceased resulted in an induction of actin synthesis reversing viral inhibitory effects. Similarly, the removal of CD resulted in virus-induced inhibition of actin synthesis. Treatment of infected cells with CD caused a delay in the onset and/or shutoff of at least five viral proteins and inhibited the amplification of polyhedrin synthesis by at least 8 hr.
在苜蓿银纹夜蛾多核多角体病毒（AcMNPV）感染期间，IPLB - Sf - 21细胞中宿主蛋白的合成受到抑制。我们在此报告，细胞松弛素D（CD），一种与肌动蛋白特异性相互作用的药物，在病毒介导的宿主蛋白肌动蛋白和微管蛋白的关闭过程中表现为拮抗剂。在未感染的细胞中，CD导致肌动蛋白合成增加，但对微管蛋白合成没有明显影响。在感染的细胞中，CD在感染早期同样增强了肌动蛋白合成，并将病毒对肌动蛋白合成的关闭延迟了14小时。微管蛋白合成的关闭被延迟了8小时。在宿主蛋白合成停止后向感染细胞中添加CD导致肌动蛋白合成的诱导，逆转了病毒的抑制作用。同样，去除CD导致病毒诱导的肌动蛋白合成抑制。用CD处理感染细胞导致至少五种病毒蛋白的出现和/或关闭延迟，并将多角体蛋白合成的扩增抑制至少8小时。
