INTERACTION OF EBV TRANSACTIVATORS WITH CELLULAR FACTORS

推动这项工作的假设是爱泼斯坦-巴尔病毒(EBV) 反式激活剂在EB病毒诱导的恶性肿瘤中是必不可少的。目标是 我们工作的一部分是揭示这些反式激活剂 功能。我们研究了EB病毒核的复杂调控 EB病毒感染过程中抗原(EBNA)的表达。EBNA蛋白 有助于B淋巴细胞永生化，因此可能有 在EBV相关淋巴瘤的发生中起作用。另一个项目 涉及EBV裂解环蛋白Z和细胞原核- 癌基因c-myb。Z蛋白负责启动开关 从EBV潜伏期到溶血性感染。我们发现c-Myb 显著增强Z激活病毒基因表达的能力。 因此，我们正在确定Z和c-Myb之间的协同作用机制。 我们正在合作研究Z表达的调节，使用一个 免疫抑制相关淋巴肿大的SCID小鼠模型。

The hypothesis driving this work is that Epstein-Barr virus (EBV) transactivators are essential for EBV-induced malignancies. The goal of our work is uncovering the mechanisms whereby these transactivators function. We study the complex regulation of Epstein-Barr virus nuclear antigen (EBNA) expression during EBV infection. EBNA proteins contribute to the immortalization of B lymphocytes, and thus may have a role in the genesis of EBV-associated lymphomas. Another project involves the EBV lytic cycle protein, Z, and the cellular proto- oncogene, c-myb. The Z protein is responsible for initiating the switch from EBV latency to lytic infection. We have discovered that c-Myb markedly enhances the ability of Z to activate viral gene expression. Thus we are determining the mechanism of synergy between Z and c-Myb. We are collaboratively studying the regulation of Z expression using a SCID mouse model of immunosuppression-associated lymphomagenesis.