Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
general
The nonstructural proteins of Nipah virus play a key role in pathogenicity in experimentally infected animals
PLoS ONE, Volume 5, No. 9, Article e12709, Year 2010
Notification
URL copied to clipboard!
Description
Nipah virus (NiV) P gene encodes P protein and three accessory proteins (V, C and W). It has been reported that all four P gene products have IFN antagonist activity when the proteins were transiently expressed. However, the role of those accessory proteins in natural infection with NiV remains unknown. We generated recombinant NiVs lacking V, C or W protein, rNiV(V2), rNiV(C2), and rNiV(W2), respectively, to analyze the functions of these proteins in infected cells and the implications in in vivo pathogenicity. All the recombinants grew well in cell culture, although the maximum titers of rNiV(V2) and rNiV(C2) were lower than the other recombinants. The rNiV(V2), rNiV(C2) and rNiV(W2) 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(V2) and rNiV(C2) but not the rNiV(W2) 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. This is the first report that identifies the molecular determinants of NiV in pathogenicity in vivo. © 2010 Yoneda et al.
Authors & Co-Authors
Georges-Courbot, Marie Claude
France, Paris
Inserm
Wild, Thomas Fabian
France, Paris
Inserm
Kai, Chieko
Japan, Tokyo
The University of Tokyo
Statistics
Citations: 71
Authors: 3
Affiliations: 2
Identifiers
Doi:
10.1371/journal.pone.0012709
ISSN:
19326203
Research Areas
Genetics And Genomics