Abstract
The working model to describe the mechanisms used to replicate the cancer-associated virus Epstein-Barr virus (EBV) is partly derived from comparisons with other members of the Herpes virus family. Many genes within the EBV genome are homologous across the herpes virus family. Published transcriptome data for the EBV genome during its lytic replication cycle show extensive transcription, but the identification of the proteins is limited. We have taken a global proteomics approach to identify viral proteins that are expressed during the EBV lytic replication cycle. We combined an enrichment method to isolate cells undergoing EBV lytic replication with SILAC-labeling coupled to mass-spectrometry and identified viral and host proteins expressed during the EBV lytic replication cycle. Amongst the most frequently identified viral proteins are two components of the DNA replication machinery, the single strand DNA binding protein BALF2, DNA polymerase accessory protein BMRF1 and both subunits of the viral ribonucleoside-diphosphate reductase enzyme (BORF2 and BaRF1). An additional 42 EBV lytic cycle proteins were also detected. This provides proteomic identification for many EBV lytic replication cycle proteins and also identifies post-translational modifications.
Highlights
Epstein-Barr virus (EBV) is associated with diverse cancers including Burkitt’s lymphoma, Hodgkin’s lymphoma, NK/T lymphomas, Nasopharyngeal carcinoma and gastric cancer [1,2,3,4,5,6,7,8,9]
To identify EBV proteins in cells undergoing lytic replication, we considered the peptides that match with an EBV protein
Two previous studies compared the proteomes in BL and primary effusion lymphoma (PEL) cells during EBV lytic cycle with the proteomes of cells during latency or to those that are refractory to entering EBV lytic cycle [33,34]
Summary
Epstein-Barr virus (EBV) is associated with diverse cancers including Burkitt’s lymphoma, Hodgkin’s lymphoma, NK/T lymphomas, Nasopharyngeal carcinoma and gastric cancer [1,2,3,4,5,6,7,8,9]. EBV within tumor cells undergoes lytic cycle replication only rarely and ~90% of EBV genes are not commonly expressed in tumors. The contributions that many other EBV lytic replication cycle genes make to the EBV lytic replication cycle are inferred through their homology with the alpha herpesvirus family [1] Several of these proteins have been detected by immunofluorescence during viral replication (e.g., [31]). Burkitt’s lymphoma cell system to enrich for cells undergoing EBV lytic replication and coupled this with SILAC-proteomics to develop a route to detect EBV proteins in Akata cells undergoing EBV lytic replication This allowed us to identify a total of 44 EBV proteins and post-translational modifications of several viral proteins
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