Wei Taiyun, Shimizu Takumi, Omura Toshihiro
National Agricultural Research Center, 3-1-1 Kannondai,Tsukuba, Ibaraki 305-8666, Japan.
Virology. 2008 Mar 15;372(2):349-56. doi: 10.1016/j.virol.2007.10.034. Epub 2007 Dec 3.
Rice dwarf virus (RDV) spreads, along actin-based filopodia, as one of the ways of its transport, from infected to non-infected cells of its vector insect via tubules that are composed of the viral nonstructural protein Pns10 and contain viral particles. An inhibitor that perturbs the endomembrane system, namely, brefeldin A, and butanedione monoxime, an inhibitor of myosin motor activity, abolished the formation of such tubules, preventing the direct cell-to-cell spread of RDV without any significant effects on the production of viral particles. The microtubule-depolymerizing drug NOC, which had a negligible effect on the formation and protrusion of such tubules from cells, did not inhibit the intercellular spread of RDV. Our observations suggest that the endomembrane system and myosin motors, but not microtubule, are required for the Pns10 tubule formation and are, therefore, involved in the secondary infection by RDV of adjacent cells.
水稻矮缩病毒(RDV)沿着肌动蛋白丝伪足扩散,这是其传播途径之一,它通过由病毒非结构蛋白Pns10组成并含有病毒粒子的小管,从其媒介昆虫的受感染细胞传播到未受感染细胞。一种干扰内膜系统的抑制剂,即布雷菲德菌素A,以及肌球蛋白运动活性抑制剂丁二酮单肟,消除了此类小管的形成,阻止了RDV的直接细胞间传播,而对病毒粒子的产生没有任何显著影响。微管解聚药物NOC对这种小管从细胞的形成和突出影响可忽略不计,并未抑制RDV的细胞间传播。我们的观察结果表明,内膜系统和肌球蛋白运动蛋白,而非微管,是Pns10小管形成所必需的,因此参与了RDV对相邻细胞的二次感染。