Proteomic alteration of equine monocyte-derived macrophages infected with equine infectious anemia virus

文献类型: 外文期刊

第一作者: Du, Cheng

作者: Du, Cheng;Liu, Hai-Fang;Lin, Yue-Zhi;Wang, Xue-Feng;Ma, Jian;Wang, Xiaojun;Zhou, Jian-Hua;Du, Cheng;Li, Yi-Jing;Zhou, Jian-Hua

作者机构:

关键词: Cellular protein;Differential expression;EIAV;iTRAQ;Macrophages;Microbiology

期刊名称:PROTEOMICS ( 影响因子:3.984; 五年影响因子:3.831 )

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收录情况: SCI

摘要: Similar to the well-studied viruses human immunodeficiency virus (HIV)-1 and simian immunodeficiency virus (SIV), equine infectious anemia virus (EIAV) is another member of the Lentivirus genus in the family Retroviridae. Previous studies revealed that interactions between EIAV and the host resulted in viral evolution in pathogenicity and immunogenicity, as well as adaptation to the host. Proteomic analysis has been performed to examine changes in protein expression and/or modification in host cells infected with viruses and has revealed useful information for virus-host interactions. In this study, altered protein expression in equine monocyte-derived macrophages (eMDMs, the principle target cell of EIAV in vivo) infected with the EIAV pathogenic strain EIAV(DLV34) (DLV34) was examined using 2D-LC-MS/MS coupled with the iTRAQ labeling technique. The expression levels of 210 cellular proteins were identified to be significantly upregulated or downregulated by infection with DLV34. Alterations in protein expression were confirmed by examining the mRNA levels of eight selected proteins using quantitative real-time reverse-transcription PCR, and by verifying the levels of ten selected proteins using parallel reaction monitoring (PRM). Further analysis of GO and Kyoto Encyclopedia of Genes and Genomes (KEGG)-Pathway enrichment demonstrated that these differentially expressed proteins are primarily related to the biological processes of oxidative phosphorylation, protein folding, RNA splicing, and ubiquitylation. Our results can facilitate a better understanding of the host response to EIAV infection and the cellular processes required for EIAV replication and pathogenesis.

分类号: Q5

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