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iTRAQ protein profile analysis of neuroblastoma (NA) cells infected with the rabies viruses rHep-Flury and Hep-dG.

Yang Y, Liu W, Yan G, Luo Y, Zhao J, Yang X, Mei M, Wu X, Guo X - Front Microbiol (2015)

Bottom Line: Bioinformatics analysis of the distinct protein suggested that glycoprotein over-expression in the attenuated RABV strain can induce activation of the interferon signaling.Furthermore, it may promote the antiviral response, MHC-I mediated antigen-specific T cell immune response, apoptosis and autophagy in an IFN-dependent manner.These findings might not only improve the understanding of the dynamics of RABV and host interaction, but also help understand the mechanisms underlying innate and adaptive immunity during RABV infection.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, South China Agricultural University Guangzhou, China.

ABSTRACT
The rabies virus (RABV) glycoprotein (G) is the principal contributor to the pathogenicity and protective immunity of RABV. In a previous work, we reported that recombinant rabies virus Hep-dG, which was generated by reverse genetics to carry two copies of the G-gene, showed lower virulence than the parental virus rHep-Flury in suckling mice with a better immune protection effect. To better understand the mechanisms underlying rabies virus attenuation and the role of glycoprotein G, isobaric tags for relative and absolute quantitation (iTRAQ) was performed to identify and quantify distinct proteins. 10 and 111 differentially expressed proteins were obtained in rHep-Flury and Hep-dG infection groups, respectively. Selected data were validated by western blot and qRT-PCR. Bioinformatics analysis of the distinct protein suggested that glycoprotein over-expression in the attenuated RABV strain can induce activation of the interferon signaling. Furthermore, it may promote the antiviral response, MHC-I mediated antigen-specific T cell immune response, apoptosis and autophagy in an IFN-dependent manner. These findings might not only improve the understanding of the dynamics of RABV and host interaction, but also help understand the mechanisms underlying innate and adaptive immunity during RABV infection.

No MeSH data available.


Related in: MedlinePlus

Network analyses of differentially expressed proteins in rabies virus HEP-dG infection group. (A) Antimicrobial response, inflammatory response, cell-to-cell signaling and interaction. (B) Cell death and survival, tissue development, cell cycle. (C) Developmental disorder, hereditary disorder, neurological disease. (D) Embryonic development, organ development, organismal development. (E) Developmental disorder, hereditary disorder, neurological disease. (F) Embryonic development, organismal development, tissue development. Red, significantly up-regulated proteins; green, significantly down-regulated proteins; and white, proteins known to be in the network but that were not identified in our study. Lines connecting the molecules indicate molecular relationships. Dashed lines indicate indirect interactions, and solid lines indicate direct interactions. The arrow styles indicate specific molecular relationships and the directionality of the interaction. More information is available in Table S3 in the Supporting Information.
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Figure 5: Network analyses of differentially expressed proteins in rabies virus HEP-dG infection group. (A) Antimicrobial response, inflammatory response, cell-to-cell signaling and interaction. (B) Cell death and survival, tissue development, cell cycle. (C) Developmental disorder, hereditary disorder, neurological disease. (D) Embryonic development, organ development, organismal development. (E) Developmental disorder, hereditary disorder, neurological disease. (F) Embryonic development, organismal development, tissue development. Red, significantly up-regulated proteins; green, significantly down-regulated proteins; and white, proteins known to be in the network but that were not identified in our study. Lines connecting the molecules indicate molecular relationships. Dashed lines indicate indirect interactions, and solid lines indicate direct interactions. The arrow styles indicate specific molecular relationships and the directionality of the interaction. More information is available in Table S3 in the Supporting Information.

Mentions: Network analysis can build and explore protein-protein interaction network involved in our proteomics data. All significantly altered proteins were subjected to network analysis. Distinct proteins in Hep-dG-infected cells were mapped to 6 specific functional networks (Figure 5, Supporting Information Table S3). Interestingly, 16 proteins in top one network, which corresponded to antimicrobial response, inflammatory response, cell-to-cell signaling and interaction, were significantly altered in Hep-dG-infected cells, but not in the rHep-Flury infection group (Figure 5A). Moreover, most of these proteins were located upstream or downstream of type I interferon (Table 1). These data suggested that infection with rabies virus Hep-dG induces a more pronounced immune response compared with that with rHep-Flury.


iTRAQ protein profile analysis of neuroblastoma (NA) cells infected with the rabies viruses rHep-Flury and Hep-dG.

Yang Y, Liu W, Yan G, Luo Y, Zhao J, Yang X, Mei M, Wu X, Guo X - Front Microbiol (2015)

Network analyses of differentially expressed proteins in rabies virus HEP-dG infection group. (A) Antimicrobial response, inflammatory response, cell-to-cell signaling and interaction. (B) Cell death and survival, tissue development, cell cycle. (C) Developmental disorder, hereditary disorder, neurological disease. (D) Embryonic development, organ development, organismal development. (E) Developmental disorder, hereditary disorder, neurological disease. (F) Embryonic development, organismal development, tissue development. Red, significantly up-regulated proteins; green, significantly down-regulated proteins; and white, proteins known to be in the network but that were not identified in our study. Lines connecting the molecules indicate molecular relationships. Dashed lines indicate indirect interactions, and solid lines indicate direct interactions. The arrow styles indicate specific molecular relationships and the directionality of the interaction. More information is available in Table S3 in the Supporting Information.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493837&req=5

Figure 5: Network analyses of differentially expressed proteins in rabies virus HEP-dG infection group. (A) Antimicrobial response, inflammatory response, cell-to-cell signaling and interaction. (B) Cell death and survival, tissue development, cell cycle. (C) Developmental disorder, hereditary disorder, neurological disease. (D) Embryonic development, organ development, organismal development. (E) Developmental disorder, hereditary disorder, neurological disease. (F) Embryonic development, organismal development, tissue development. Red, significantly up-regulated proteins; green, significantly down-regulated proteins; and white, proteins known to be in the network but that were not identified in our study. Lines connecting the molecules indicate molecular relationships. Dashed lines indicate indirect interactions, and solid lines indicate direct interactions. The arrow styles indicate specific molecular relationships and the directionality of the interaction. More information is available in Table S3 in the Supporting Information.
Mentions: Network analysis can build and explore protein-protein interaction network involved in our proteomics data. All significantly altered proteins were subjected to network analysis. Distinct proteins in Hep-dG-infected cells were mapped to 6 specific functional networks (Figure 5, Supporting Information Table S3). Interestingly, 16 proteins in top one network, which corresponded to antimicrobial response, inflammatory response, cell-to-cell signaling and interaction, were significantly altered in Hep-dG-infected cells, but not in the rHep-Flury infection group (Figure 5A). Moreover, most of these proteins were located upstream or downstream of type I interferon (Table 1). These data suggested that infection with rabies virus Hep-dG induces a more pronounced immune response compared with that with rHep-Flury.

Bottom Line: Bioinformatics analysis of the distinct protein suggested that glycoprotein over-expression in the attenuated RABV strain can induce activation of the interferon signaling.Furthermore, it may promote the antiviral response, MHC-I mediated antigen-specific T cell immune response, apoptosis and autophagy in an IFN-dependent manner.These findings might not only improve the understanding of the dynamics of RABV and host interaction, but also help understand the mechanisms underlying innate and adaptive immunity during RABV infection.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, South China Agricultural University Guangzhou, China.

ABSTRACT
The rabies virus (RABV) glycoprotein (G) is the principal contributor to the pathogenicity and protective immunity of RABV. In a previous work, we reported that recombinant rabies virus Hep-dG, which was generated by reverse genetics to carry two copies of the G-gene, showed lower virulence than the parental virus rHep-Flury in suckling mice with a better immune protection effect. To better understand the mechanisms underlying rabies virus attenuation and the role of glycoprotein G, isobaric tags for relative and absolute quantitation (iTRAQ) was performed to identify and quantify distinct proteins. 10 and 111 differentially expressed proteins were obtained in rHep-Flury and Hep-dG infection groups, respectively. Selected data were validated by western blot and qRT-PCR. Bioinformatics analysis of the distinct protein suggested that glycoprotein over-expression in the attenuated RABV strain can induce activation of the interferon signaling. Furthermore, it may promote the antiviral response, MHC-I mediated antigen-specific T cell immune response, apoptosis and autophagy in an IFN-dependent manner. These findings might not only improve the understanding of the dynamics of RABV and host interaction, but also help understand the mechanisms underlying innate and adaptive immunity during RABV infection.

No MeSH data available.


Related in: MedlinePlus