2010 Fiscal Year Final Research Report

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

Research Project

Project/Area Number	21790439
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Virology
Research Institution	The University of Tokyo
Principal Investigator	YONEDA Misako The University of Tokyo, 医科学研究所, 准教授 (40361620)
Project Period (FY)	2009 – 2010
Keywords	ニパウイルス / 病原性発現 / アクセサリー蛋白
Research Abstract	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.