摘要
ＨＨＶ－６在体外可以激活ＨＩＶＬＴＲ引导的基因表达［１］，其基因组中一基因片段Ｂ７０１已被证明与这种激活作用有关［２］．Ｂ７０１编码１４３个氨基酸的蛋白质，可与ＨＨＶ－６基因组中其它基因片段协同作用提高对ＨＩＶＬＴＲ的激活效力．对Ｂ７０１进行缺失突变，得到突变体ＲＳＶ－Ｂ７０１－ｄ１（３′端缺失１８１个ｂｐ）、ＲＳＶ－Ｂ７０１－ｄ６（３′端缺失３５３个ｂｐ），将这两个缺失突变体分别与ＨＩＶ－Ｌｕｃ共转染受体细胞，通过ＬＵＣ活性分析发现，缺失突变体ｄ１、ｄ６不但仍具有激活能力，而且ｄ６的激活能力要远远大于ｄ１．二级结构预测初步揭示了Ｂ７０１对ＨＩＶ－ＬＴＲ的反式激活作用机制，为阐明ＨＨＶ－６基因产物与ＡＩＤＳ的病理关系提供了依据．
Human Herpesvirus (HHV 6) can trans activate the human immunodeficiency virus (HIV) promoter and accelerate cytopathetic effects in HIV infected human T cells. A gene segment B701 showed high trans active ability in vitro. In this study, we demonstrated that 2 deletions of B701 can trans activate the HIV promoter in contransfected CV 1 cell line. All these deletions cannot trans activate HIV promoter constructs containing a deleted or mutant enhancer site. We also identified that B701 can work together with other gene segments that can trans activate HIV 1 LTR in vitro to increase the HIV LTR directed Luc gene expression dramatically.
出处
《南开大学学报（自然科学版）》
CAS
CSCD
北大核心
1999年第1期7-13,共7页
Acta Scientiarum Naturalium Universitatis Nankaiensis
基金
国家科委基础研究高技术司资助
