Watanabe Shinji, Noda Takeshi, Halfmann Peter, Jasenosky Luke, Kawaoka Yoshihiro
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI, USA.
J Infect Dis. 2007 Nov 15;196 Suppl 2:S284-90. doi: 10.1086/520582.
The roles of Ebola virus (EBOV) VP24 in nucleocapsid (NC) formation and the effect of VP24 on transcription and replication of the viral genome during NC formation remain unknown. We therefore examined the effect of VP24 on the expression of a reporter gene (luciferase), viral RNA, and messenger RNA from the EBOV minigenome. VP24 inhibited the expression of luciferase and both RNAs in a dose-dependent manner, suggesting that VP24 inhibits transcription and replication of the EBOV genome. By contrast, FLAG-tagged VP24, which cannot support NC-like structure formation, did not appreciably decrease luciferase expression, indicating that association of VP24 with the ribonucleoprotein complex is required for inhibition. Glycoprotein and VP40 did not affect VP24-mediated inhibition of transcription and replication. Together, these results suggest that VP24 reduces transcription and replication of the EBOV genome by direct association with the ribonucleoprotein complex in virus-infected cells.
埃博拉病毒(EBOV)VP24在核衣壳(NC)形成中的作用以及VP24在NC形成过程中对病毒基因组转录和复制的影响尚不清楚。因此,我们研究了VP24对来自埃博拉病毒微型基因组的报告基因(荧光素酶)、病毒RNA和信使RNA表达的影响。VP24以剂量依赖的方式抑制荧光素酶和两种RNA的表达,表明VP24抑制埃博拉病毒基因组的转录和复制。相比之下,不能支持类NC结构形成的带有FLAG标签的VP24并没有明显降低荧光素酶的表达,这表明VP24与核糖核蛋白复合物的结合是抑制所必需的。糖蛋白和VP40不影响VP24介导的转录和复制抑制。这些结果共同表明,VP24通过与病毒感染细胞中的核糖核蛋白复合物直接结合来减少埃博拉病毒基因组的转录和复制。