Characterization of the antiviral and inflammatory responses against Nipah virus in endothelial cells and neurons.
Nipah virus (NiV) is a highly pathogenic paramyxovirus which causes fatal encephalitis in up to 75% of infected humans. Endothelial cells and neurons are important cellular targets in the pathogenesis of this disease. In this study, viral replication and the innate immune responses to NiV in these cell types were measured. NiV infected endothelial cells generated a functionally robust IFN-beta response, which correlated with localization of the NiV W protein to the cytoplasm. There was no antiviral response detected in infected neuronal cells. NiV infection of endothelial cells induced a significant increase in secreted inflammatory chemokines, which corresponded with the increased ability of infected cell supernatants to induce monocyte and T-lymphocyte chemotaxis. These results suggest that pro-inflammatory chemokines produced by NiV infected primary endothelial cells in vitro is consistent with the prominent vasculitis observed in infections, and provide initial molecular insights into the pathogenesis of NiV in physiologically relevant cells types.
Lo
Michael K
MK
Measles, Mumps, Rubella, and Herpesvirus Laboratory Branch, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. mko2@cdc.gov
Miller
David
D
Aljofan
Mohammad
M
Mungall
Bruce A
BA
Rollin
Pierre E
PE
Bellini
William J
WJ
Rota
Paul A
PA
D002478:Cells, Cultured; D018925:Chemokines / Q000378:metabolism; D002633:Chemotaxis; D042783:Endothelial Cells / Q000821:virology*; D006801:Humans; D016899:Interferon-beta / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D009474:Neurons / Q000821:virology*; D045405:Nipah Virus / Q000276:immunology* / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology; D014779:Virus Replication
D018925:Chemokines; D016899:Interferon-beta