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Global quantitative proteomic analysis profiles host protein expression in response to Sendai virus infection.

Authors :
Zhu SL
Chen X
Wang LJ
Wan WW
Xin QL
Wang W
Xiao G
Zhang LK
Source :
Proteomics [Proteomics] 2017 Mar; Vol. 17 (5).
Publication Year :
2017

Abstract

Sendai virus (SeV) is an enveloped nonsegmented negative-strand RNA virus that belongs to the genus Respirovirus of the Paramyxoviridae family. As a model pathogen, SeV has been extensively studied to define the basic biochemical and molecular biologic properties of the paramyxoviruses. In addition, SeV-infected host cells were widely employed to uncover the mechanism of innate immune response. To identify proteins involved in the SeV infection process or the SeV-induced innate immune response process, system-wide evaluations of SeV-host interactions have been performed. cDNA microarray, siRNA screening and phosphoproteomic analysis suggested that multiple signaling pathways are involved in SeV infection process. Here, to study SeV-host interaction, a global quantitative proteomic analysis was performed on SeV-infected HEK 293T cells. A total of 4699 host proteins were quantified, with 742 proteins being differentially regulated. Bioinformatics analysis indicated that regulated proteins were mainly involved in "interferon type I (IFN-I) signaling pathway" and "defense response to virus," suggesting that these processes play roles in SeV infection. Further RNAi-based functional studies indicated that the regulated proteins, tripartite motif (TRIM24) and TRIM27, affect SeV-induced IFN-I production. Our data provided a comprehensive view of host cell response to SeV and identified host proteins involved in the SeV infection process or the SeV-induced innate immune response process.<br /> (© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Details

Language :
English
ISSN :
1615-9861
Volume :
17
Issue :
5
Database :
MEDLINE
Journal :
Proteomics
Publication Type :
Academic Journal
Accession number :
28067018
Full Text :
https://doi.org/10.1002/pmic.201600239