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背景与目的:Epstein-Barr病毒(Epstein-Barrvirus,EBV)以潜伏状态存在于Burkitt’s淋巴瘤(Burkitt’s lymphoma,BL)细胞中,其基因表达呈高度限制模式,只有少数肿瘤细胞存在病毒裂解性复制。BL细胞株可被诱导进入病毒裂解周期,通过刺激表面免疫球蛋白分子启动病毒复制过程。此过程中,有许多EBV基因表达,这些基因可能影响宿主基因的表达。本实验目的在于鉴定BL细胞中由EBV所调节的宿主基因及由表面IgG连接所调节的宿主基因。方法:利用微阵列检测EBV阳性Akata细胞和EBV阴性AK31细胞中差异性表达的基因。结果:Akata和AK31细胞中共有91个人类基因呈差异性表达,细胞受刺激进入裂解性复制后,检测到198个差异性表达基因。其中myd88基因的差异性表达与TLR9信号通路受损有关。结论:EBV下调了在裂解周期激活早期阶段由表面Ig交联作用所调节的大部分基因。这些基因与细胞存活、信号转导、转录控制以及可能调节B淋巴细胞和其他细胞(如可能影响病毒复制的HDAC4)EBV转化的免疫应答过程有关。
BACKGROUND & OBJECTIVE: Epstein-Barr virus (Epstein-Barr virus) is latent in Burkitt’s lymphoma (BL) cells. Epstein-Barr virus (HB) gene expression is highly restricted and only a few tumor cells have viral lytic replication. The BL cell line can be induced into the viral lysis cycle to initiate the viral replication process by stimulating surface immunoglobulin molecules. In this process, there are many EBV gene expression, these genes may affect the host gene expression. The aim of this experiment was to identify host genes regulated by EBV in BL cells and host genes regulated by surface IgG ligation. Methods: Microarray was used to detect differentially expressed genes in EBV-positive Akata cells and EBV-negative AK31 cells. RESULTS: A total of 91 human genes were differentially expressed in Akata and AK31 cells, and 198 differentially expressed genes were detected after the cells were stimulated into lytic replication. Among them, the differential expression of myd88 gene is related to the impaired TLR9 signaling pathway. Conclusions: EBV down-regulates most of the genes that are regulated by surface Ig cross-linking during the early stages of activation of the cleavage cycle. These genes are involved in cell survival, signal transduction, transcriptional control and the immune response that may regulate the EBV transformation of B lymphocytes and other cells, such as HDAC4, which may affect viral replication.