Abstract
Effects of the Epstein-Barr virus (EBV) on cellular protein expression are essential for viral pathogenesis. To characterize the cellular response to EBV infection, differential proteomes of gastric epithelial AGS cells were analyzed with two-dimensional gel electrophoresis (2-DE) followed by matrix-assisted laser desorption/ionization- time of flight (MALDI-TOF) and liquid chromatography electrospray/ionization ion trap (LC-ESI-IT) mass spectrometry identification. Mass spectrometry identified 9 altered cellular proteins, including 5 up-regulated and 4 down-regulated proteins after EBV infection. Notably 2-DE analysis revealed that EBV infection induced increased expression of heat shock cognate 71 kDa protein, actin cytoplasmic 1, pyridoxine-5'-phosphate oxidase, caspase 9, and t-complex protein 1 subunit alpha. In addition, EBV infection considerably suppressed those cellular proteins of zinc finger protein 2, cyclin-dependent kinase 2, macrophage-capping protein, and growth/ differentiation factor 11. Furthermore, the differential expressional levels of partial proteins (cyclin-dependent kinase 2 and caspase 9) were confirmed by Western blot analysis.Thus, this work effectively provided useful protein-related information to facilitate further investigation of the mechanisms underlying EBV infection and pathogenesis.
Highlights
Epstein-Barr virus is a member of the herpesvirus family and infects more than 90% of population worldwide (Epstein et al, 1964)
The goal of this study was to analyze the effects of Epstein-Barr virus (EBV) infection on cellular protein expression in order to gain further insight into EBV pathogenesis
We obtained an overview of the altered protein expressions of host cells responding to EBV infection
Summary
Epstein-Barr virus is a member of the herpesvirus family and infects more than 90% of population worldwide (Epstein et al, 1964). It causes infectious mononucleosis and has been reported to be associated with various lymphoid and epithelial malignancies, including Burkitt’s lymphoma, Hodgkin’s disease, nasopharyngeal carcinoma, gastric carcinoma, etc (Young et al, 2004). EBVaGC is a unique type of GC, consisting of the monoclonal growth of EBV-infected epithelial cells, and it represents a model of virus-host interactions leading to carcinoma (Fukayama et al, 2008). The mRNA abundance is not always consistent with the protein level (Gygi et al, 1999), and viral infection results in post-translational modifications without affecting their transcription rates. Proteomic analyses have been employed to better understand host alterations to virus infection
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