Geng Y, Kashanchi F, Wood C
Department of Microbiology, University of Kansas, Lawrence 66045.
Virology. 1992 Apr;187(2):832-6. doi: 10.1016/0042-6822(92)90489-c.
Bovine immunodeficiency-like virus (BIV) is a recently identified lentivirus that infects cattle. The virus has structural and genetic similarities to human HIV. The present study demonstrates that BIV can be activated by bovine herpesvirus type 1 (BHV-1), a pathogen frequently associated with cattle diseases. Activation of BIV expression can be detected as increased BIV reverse transcriptase activity, increased in the number of syncytia induced by BIV, and increased in the steady state level of BIV-specific RNA upon BHV-1 super-infection. Additional transactivation studies using the BIV-LTR (long terminal repeat) were conducted. The BIV-LTR was linked to the chloramphenicol acetyl transferase gene (CAT) and transfected into bovine cell cultures in order to quantitate the levels of BIV-LTR expression. When the transfected cells were infected by BHV-1, there was an increase in CAT expression, indicating transactivation of the BIV-LTR by BHV-1. Most of the transactivation activities were abolished with an LTR construct that has deleted the NF-kappa B-like sequence located in the U3 region of the LTR. In order to further demonstrate that activation of the BIV-LTR involves factors that may bind to the LTR sequences, gel retardation assays were carried out using the BIV-LTR U3 region as probe. Our results showed that BHV-1 infection resulted in an induction of factor(s) that binds to the NF-kappa B-like sequence on the BIV-LTR. This suggests that transactivation of BIV by BHV-1 may be mediated by a bovine NF-kappa B-like protein that binds to the target sequence in the BIV promoter region.
牛免疫缺陷样病毒(BIV)是一种最近发现的感染牛的慢病毒。该病毒在结构和基因上与人类HIV相似。本研究表明,BIV可被1型牛疱疹病毒(BHV - 1)激活,BHV - 1是一种常与牛疾病相关的病原体。BIV表达的激活可通过BIV逆转录酶活性增加、BIV诱导的合胞体数量增加以及BHV - 1超感染后BIV特异性RNA稳态水平增加来检测。使用BIV长末端重复序列(LTR)进行了额外的反式激活研究。将BIV - LTR与氯霉素乙酰转移酶基因(CAT)连接,并转染到牛细胞培养物中,以定量BIV - LTR的表达水平。当转染细胞被BHV - 1感染时,CAT表达增加,表明BHV - 1对BIV - LTR进行了反式激活。大多数反式激活活性在一个删除了位于LTR U3区域的NF - κB样序列的LTR构建体中被消除。为了进一步证明BIV - LTR的激活涉及可能与LTR序列结合的因子,使用BIV - LTR U3区域作为探针进行了凝胶阻滞试验。我们的结果表明,BHV - 1感染导致诱导了与BIV - LTR上的NF - κB样序列结合的因子。这表明BHV - 1对BIV的反式激活可能由一种与BIV启动子区域靶序列结合的牛NF - κB样蛋白介导。