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

我们利用反向基因构建的缺失辅助蛋白的重组病毒，研究了辅助蛋白在新城疫病毒致病中的作用。虽然rNiV(V-)和rNiV(C-)的最大滴度低于其他重组体，但所有重组体在细胞培养中都生长良好。RNiV(V-)、rNiV(C-)和rNiV(W-)对干扰素应答和亲本rNiV均有抑制作用，说明各辅助蛋白的缺乏对感染细胞中干扰素信号的抑制没有显著影响。在实验感染的金黄地鼠中，rNiV(V-)和rNiV(C-)而不是rNiV(W-)病毒的毒力显著降低。这些结果表明，V蛋白和C蛋白在新城疫病毒致病中起关键作用，并且这些作用不依赖于它们的干扰素拮抗剂活性。

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.