ABSTRACT
Objective To compare the different expression of EBNA-1 in the normal human lymphocytes and in the EBV-induced lymphomas so as to provide the basis for studying the mechanism of the EB virus-induced lymphoma. Methods Animal model of EBV-induced lymphoma was constructed in SCID mice. EBNA-1 gene expression level was detected by real-time PCR and Western blot. Results EBV-induced lymphomas in animal model were replicated. EBNA-1 gene was expressed both in normal human lymphoma cells and 3 EBV-induced lymphoma cells. In EBV-induced lymphoma cells , the expression was up-regulated 11 683 times than in normal lymphocytes. Western blot results showed that the expression of EBNA-1 protein in induced lymphoma cells increased significantly compared with that in normal lymphocytes. Conclusions EBNA-1 expression in EBV-induced lymphoma cells is up-regulated than in normal lymphocytes. EBNA-1 may play an important role in the development of EBV-induced lymphoma.
ABSTRACT
Epstein-Barr virus( EBV )is a ubiquitous human gamma-1 herpesvirus,which is associated with human malignancies,such as nasopharyngeal carcinoma,Burkitt's lymphoma and Hodgkin lymphoma.Based on the polymorphism of amino acids in the polymorphic region of EBV genome,it can be classified into different subtypes/variants.By now,whether the subtypes/variants of EBV preferentially is associated with particular malignancies or represent geographical polymorphism remains controversial.This review summarized the literature on sequence variation in EBV genes,focusing on LMP-1,EBNA-1,and BZLF-1 and their distribution by geography and disease.
ABSTRACT
BACKGROUND: Epstein-Barr virus associated gastric lymphoepithelioma-like carcinoma (LELC) is characterized by the intensive infiltration of lymphoid cells, the presence of EBV, and the better prognosis over typical adenocarcinoma. Thus, it was assumable that viral latent proteins may be responsible for the recruitment of a certain T cell repertoire to EBV-associated gastric carcinoma. METHODS: To examine above possibility, EBV gene expression in gastric carcinoma tissues and usage of TCR among the tumor infiltrating lymphocytes were analyzed. RESULTS: EBV specific DNA and EBERs RNA were detected in 4 out of 30 patients. RT-PCR analysis revealed that all 4 of EBV-positive tumor tissues expressed EBNA1 mRNA and BARTs and LMP2a was detected only one sample out of 4. However, the EBNA2 and LMP-1 transcripts were not detected in these tissues. CD8+ T cells were the predominant population of infiltrating lymphocytes in the EBV-positive gastric carcinoma. According to spectra type analysis of infiltrating T cells, 10 predominant bands were detected by TCR Vbeta CDR3 specific RT-PCR from 4 EBV-positive tumor tissues. Sequence analysis of these bands revealed oligoclonal expansion of T cells. CONCLUSION: These findings suggest that clonally expanded T cells in vivo might be a population of cytotoxic T cells reactive to EBV-associated gastric carcinoma.