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

Proteomics. 2017 Mar;17(5). doi: 10.1002/pmic.201600239.

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.

Keywords: Innate immune response; Quantitative proteomics; Sendai virus; Virus-host interaction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytoplasm / chemistry
  • Cytoplasm / metabolism
  • Cytoplasm / virology
  • HEK293 Cells / virology
  • Host-Pathogen Interactions / physiology*
  • Humans
  • Interferon Type I / genetics
  • Interferon Type I / metabolism
  • Nuclear Proteins / analysis
  • Nuclear Proteins / metabolism
  • Polymerase Chain Reaction / methods
  • Proteome / analysis*
  • Proteome / genetics
  • Proteome / metabolism
  • Proteomics / methods
  • Reproducibility of Results
  • Respirovirus Infections / metabolism*
  • Respirovirus Infections / virology
  • Sendai virus / pathogenicity*
  • Transcription Factors / metabolism
  • Tripartite Motif Proteins / metabolism
  • Ubiquitin-Protein Ligases / metabolism
  • Virus Replication

Substances

  • Interferon Type I
  • Nuclear Proteins
  • Proteome
  • Transcription Factors
  • Tripartite Motif Proteins
  • TRIM25 protein, human
  • Ubiquitin-Protein Ligases