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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．
HHV-6 can activate HIVLTR-induced gene expression in vitro [1], and a gene fragment B701 in its genome has been shown to be involved in this activation [2]. B701 encodes a protein of 143 amino acids which synergizes with other gene fragments in the HHV-6 genome to enhance the activation of HIVLTR. The deletion mutation of B701 resulted in the deletion of RSV-B701-d1 (181 bp at the 3 ’end) and RSV-B701-d6 (353 bp at the 3’ end) Luc co-transfected into recipient cells, LUC activity analysis found that the deletion mutant d1, d6 not only still have the ability to activate, and d6 activation is much greater than d1. Secondary structure prediction initially revealed the mechanism of transactivation of HIV-LTR by B701 and provided a basis for elucidating the pathological relationship between HHV-6 gene product and AIDS.