Shimizu N, Takada K
Department of Virology and Parasitology, Yamaguchi University School of Medicine, Japan.
J Virol. 1993 Jun;67(6):3240-5. doi: 10.1128/JVI.67.6.3240-3245.1993.
The induction of the viral lytic cycle in latently Epstein-Barr virus (EBV)-infected B cells is initiated by activation of the BZLF1 gene, whose expression is sufficient to disrupt EBV latency, suggesting that BZLF1 acts as the switch to change from a latent to a lytic replicative cycle. In the present studies, a series of deletion plasmids encompassing positions bp -552 to +12 of the BZLF1 promoter were constructed and tested for their response to anti-immunoglobulin (anti-Ig), an inducer of the viral lytic cycle, upon transfection into EBV-negative and -positive lymphoid cells. The promoter consisted of three functionally distinct regions. Region I (bp -552 to -221) had a negative influence on promoter activity; its deletion made the promoter highly responsive to anti-Ig. Region II (bp -203 to -177) was important for conferring responsiveness to anti-Ig. The response to anti-Ig did not require the presence of the EBV genome or EBV gene products. This sequence also enhanced expression of the chloramphenicol acetyltransferase (cat) gene from the simian virus 40 promoter in response to anti-Ig, even when inserted downstream of the cat gene. Region III (-134 to -116) was a positive element that was transactivated by the BZLF1 gene product.
在潜伏感染爱泼斯坦-巴尔病毒（EBV）的B细胞中，病毒裂解周期的诱导是由BZLF1基因的激活引发的，该基因的表达足以破坏EBV潜伏期，这表明BZLF1作为从潜伏复制周期转变为裂解复制周期的开关。在本研究中，构建了一系列包含BZLF1启动子-552至+12碱基对位置的缺失质粒，并在转染到EBV阴性和阳性淋巴细胞后，检测它们对病毒裂解周期诱导剂抗免疫球蛋白（anti-Ig）的反应。该启动子由三个功能不同的区域组成。区域I（-552至-221碱基对）对启动子活性有负面影响；其缺失使启动子对抗Ig高度敏感。区域II（-203至-177碱基对）对于赋予对抗Ig的反应性很重要。对抗Ig的反应不需要EBV基因组或EBV基因产物的存在。即使插入到氯霉素乙酰转移酶（cat）基因下游，该序列也能增强猿猴病毒40启动子驱动的cat基因对抗Ig的表达。区域III（-134至-116）是一个正性元件，可被BZLF1基因产物反式激活。
