爱泼斯坦-巴尔病毒BZLF1基因产物激活人类免疫缺陷病毒1型5'长末端重复序列。
The Epstein-Barr virus BZLF1 gene product activates the human immunodeficiency virus type 1 5' long terminal repeat.
作者信息
Mallon R, Borkowski J, Albin R, Pepitoni S, Schwartz J, Kieff E
机构信息
Department of Antiviral Chemotherapy, Schering-Plough Research, Bloomfield, New Jersey 07003.
出版信息
J Virol. 1990 Dec;64(12):6282-5. doi: 10.1128/JVI.64.12.6282-6285.1990.
Abstract
The Epstein-Barr virus immediate-early gene product BZLF1 transactivates the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR). The BZLF1 gene product caused an 18-fold increase in beta-galactosidase activity from an HIV-1 LTR lacZ expression vector, whereas the HIV-1 transactivator tat caused a 44-fold increase in beta-galactosidase activity. When cells were transfected with both BZLF1 (pEBV-Z) and tat (pTAT3) expression vectors, as well as HIV-1 LTR lacZ plasmid (pLRON), a 214-fold increase in beta-galactosidase activity was observed. This result suggests a synergistic effect of BZLF1 and tat on HIV-1 LTR-directed lacZ gene expression. Analysis of quantitative BZLF1 and tat requirements for maximal HIV-1 LTR activation indicates that BZLF1 does not reduce the amount of tat required for maximal LTR activation, as would be expected if the BZLF1 synergistic effect was due to increased tat gene expression. Thus, coordinate effects of BZLF1 and tat on the HIV-1 LTR or its transcript are probably responsible for synergistic HIV-1 LTR activation.
摘要
爱泼斯坦-巴尔病毒即刻早期基因产物BZLF1可反式激活1型人类免疫缺陷病毒（HIV-1）的长末端重复序列（LTR）。BZLF1基因产物使来自HIV-1 LTR lacZ表达载体的β-半乳糖苷酶活性增加了18倍，而HIV-1反式激活因子tat使β-半乳糖苷酶活性增加了44倍。当用BZLF1（pEBV-Z）和tat（pTAT3）表达载体以及HIV-1 LTR lacZ质粒（pLRON）转染细胞时，观察到β-半乳糖苷酶活性增加了214倍。这一结果表明BZLF1和tat对HIV-1 LTR指导的lacZ基因表达具有协同作用。对BZLF1和tat激活HIV-1 LTR所需的定量分析表明，BZLF1不会减少最大程度激活LTR所需的tat量，而如果BZLF1的协同作用是由于tat基因表达增加所预期的那样，则会减少。因此，BZLF1和tat对HIV-1 LTR或其转录本的协同作用可能是HIV-1 LTR协同激活的原因。
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