The role of viral proteins in the pathogenicity of Nipah virus.

利用反向遗传学方法构建了缺失辅助蛋白的重组病毒，研究了辅助蛋白在NiV致病性中的作用，结果表明，重组病毒在细胞培养中生长良好，但rNiV（V-）和rNiV（C-）的最高滴度较低。rNiV（V-）、rNiV（C-）和rNiV（W-）抑制IFN应答以及亲本rNiV，从而表明缺乏每种辅助蛋白不会显著影响感染细胞中IFN信号传导的抑制。在实验感染的金黄仓鼠中，rNiV（V-）和rNiV（C-）而不是rNiV（W-）病毒显示毒力显著降低。这些结果表明，V和C蛋白在NiV的致病性中起关键作用，并且这些作用与它们的IFN-拮抗剂活性无关。

We investigated the role of the accessory proteins in the NiV pathogenicity, using recombinant viruses lacking the accessory proteins which were constructed by reverse genetics.All the recombinants grew well in cell culture, although the maximum titers of rNiV(V-) and rNiV(C-) were lower than the other recombinants. The rNiV(V-), rNiV(C-) and rNiV(W-) suppressed the IFN response as well as the parental rNiV, thereby indicating that the lack of each accessory protein does not significantly affect the inhibition of IFN signaling in infected cells. In experimentally infected golden hamsters, rNiV(V-) and rNiV(C-) but not the rNiV(W-) virus showed a significant reduction in virulence. These results suggest that V and C proteins play key roles in NiV pathogenicity, and the roles are independent of their IFN-antagonist activity.