Bednarik D P, Mosca J D, Raj N B
J Virol. 1987 Apr;61(4):1253-7. doi: 10.1128/JVI.61.4.1253-1257.1987.
When Vero or murine cells were stably transfected with the human immunodeficiency virus (HIV) long terminal repeat (LTR) that directs the chloramphenicol acetyltransferase (CAT) gene (pU3R-III-CAT), expression was suppressed. Treatment with the nucleoside analog 5-azacytidine (5-azaC) restored CAT expression. S1 nuclease analysis and a nuclear run-on assay demonstrated that activation of the latent HIV LTR by 5-azacytidine occurred at the transcriptional level. Southern blot analysis demonstrated that this activation was due to the demethylation of cytosine residues in the LTR enhancer. Thus, the HIV LTR appears to be susceptible to transcriptional inactivation by methylation, a process that is proposed to play a modulatory role in viral latency.
当用人免疫缺陷病毒（HIV）长末端重复序列（LTR）稳定转染Vero细胞或鼠细胞，该LTR指导氯霉素乙酰转移酶（CAT）基因（pU3R-III-CAT）时，表达受到抑制。用核苷类似物5-氮杂胞苷（5-azaC）处理可恢复CAT表达。S1核酸酶分析和核转录分析表明，5-氮杂胞苷对潜伏HIV LTR的激活发生在转录水平。Southern印迹分析表明，这种激活是由于LTR增强子中胞嘧啶残基的去甲基化。因此，HIV LTR似乎易受甲基化导致的转录失活影响，这一过程被认为在病毒潜伏中起调节作用。
