Jones C, Delhon G, Bratanich A, Kutish G, Rock D
Department of Microbiology, University of Mississippi Medical Center, Jackson 39216-4505.
J Virol. 1990 Mar;64(3):1164-70. doi: 10.1128/JVI.64.3.1164-1170.1990.
As a transcriptional promoter in primary cultures of sensory ganglionic neurons, DNA sequences near the 5' terminus of the latency-related (LR) gene of bovine herpesvirus 1 were at least 10 times more efficient than the simian virus 40 early promoter-enhancer. In contrast, as a promoter in bovine, rodent, or monkey cells, the LR promoter was approximately six times less efficient than the simian virus 40 early promoter-enhancer. The LR promoter had strict orientation preferences in neurons and all other mammalian cell lines tested. Removal of a 146-base-pair XhoI fragment from the LR promoter resulted in stimulation of LR promoter activity in bovine cells but not rabbit neurons, monkey fibroblasts, or rodent cells. LR promoter activity in bovine cells is stimulated by bovine herpesvirus 1 lytic infection, suggesting that viral gene products or virus-induced factors positively regulate the expression of the LR gene. A synthetic glucocorticoid, dexamethasone, repressed LR promoter activity in bovine cells. These results imply that a variety of factors can influence the expression of the LR gene during latent infections of neurons as well as during the lytic infection cycle.
作为感觉神经节神经元原代培养中的转录启动子，牛疱疹病毒1潜伏相关（LR）基因5'末端附近的DNA序列比猴病毒40早期启动子 - 增强子的效率至少高10倍。相比之下，作为牛、啮齿动物或猴细胞中的启动子，LR启动子的效率比猴病毒40早期启动子 - 增强子低约6倍。LR启动子在神经元和所有其他测试的哺乳动物细胞系中具有严格的方向偏好。从LR启动子中去除一个146个碱基对的XhoI片段会导致牛细胞中LR启动子活性的刺激，但兔神经元、猴成纤维细胞或啮齿动物细胞中则不会。牛疱疹病毒1的裂解感染会刺激牛细胞中的LR启动子活性，这表明病毒基因产物或病毒诱导的因子正向调节LR基因的表达。合成糖皮质激素地塞米松会抑制牛细胞中的LR启动子活性。这些结果表明，在神经元潜伏感染以及裂解感染周期中，多种因素可以影响LR基因的表达。
