Promoter sequences required for reactivation of Epstein-Barr virus from latency
Promoter sequences required for reactivation of Epstein-Barr virus from latency
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DOI：
10.1128/jvi.76.20.10282-10289.2002
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发表时间：
2002-10-01
影响因子：
5.4
通讯作者：
Farrell, PJ
中科院分区：
文献类型：
--
作者：
Binné, UK;Amon, W;Farrell, PJ
Akata Burkitt淋巴瘤细胞中稳定转染oriP质粒的荧光素酶报告基因系统通过与抗免疫球蛋白交联，提供了对BZLF 1 Zp启动子响应B细胞受体（BCR）激活的定量测定。在该系统中，启动子活性的详细动力学研究是可能的。以前报道的启动子元件上游-221从转录开始和ZIIR序列对Zp启动子几乎没有影响，但ZI和ZIIIA元件是必不可少的早期激活。ZIIIB元件介导自激活。ZV阻遏序列的突变大大增加了启动子的诱导，但没有使其组成型活性。Zp转录响应BCR交联下降后几个小时，这种下降减少和延迟阿昔洛韦或膦酰基乙酸，表明病毒DNA复制或晚期病毒基因可以发挥作用的Zp启动子的开关关闭。LMP 1蛋白的晚期表达可能是原因之一。
A luciferase reporter system with stably transfected oriP plasmids in Akata Burkitt's lymphoma cells provides a quantitative assay for the BZLF1 Zp promoter in response to B-cell receptor (BCR) activation by cross-linking with anti -immunoglobulin. In this system, detailed kinetic studies of promoter activity are possible. Previously reported promoter elements upstream of -221 from the transcription start and the ZIIR sequence had little effect on the Zp promoter, but the ZI and ZIIIA elements were essential for early activation. The ZIIIB element mediates autoactivation. Mutation of the ZV repressor sequence greatly increased the induction of the promoter but did not make it constitutively active. Zp transcription in response to BCR cross-linking declined after a few hours; this decline was reduced and delayed by acyclovir or phosphonoacetic acid, indicating that viral DNA replication or a late viral gene can play a role in the switch off of the Zp promoter. Late expression of the LMP1 protein may account for this.