Duh E J, Maury W J, Folks T M, Fauci A S, Rabson A B
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.
Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8. doi: 10.1073/pnas.86.15.5974.
Expression of human immunodeficiency virus type 1 (HIV-1) can be activated in a chronically infected T-cell line (ACH2 cells) by a cytokine, human tumor necrosis factor alpha (TNF-alpha). TNF-alpha treatment of ACH2 cells resulted in an increase in steady-state levels of HIV RNA and HIV transcription. Gel mobility shift assays demonstrated that the transcriptional activation of the HIV long terminal repeat (LTR) by TNF-alpha was associated with the induction of a nuclear factor(s) binding to the NF-kappa B sites in the LTR. Deletion of the NF-kappa B sites from the LTR eliminated activation by TNF-alpha in T cells transfected with plasmids in which the HIV LTR directed the expression of the bacterial chloramphenicol acetyltransferase gene. Thus, TNF-alpha appears to activate HIV RNA and virus production by ACH2 cells through the induction of transcription-activating factors that bind to the NF-kappa B sequences in the HIV LTR.
细胞因子人肿瘤坏死因子α（TNF-α）可激活慢性感染的T细胞系（ACH2细胞）中1型人类免疫缺陷病毒（HIV-1）的表达。用TNF-α处理ACH2细胞导致HIV RNA稳态水平和HIV转录增加。凝胶迁移率变动分析表明，TNF-α对HIV长末端重复序列（LTR）的转录激活与诱导一种或多种与LTR中NF-κB位点结合的核因子有关。从LTR中删除NF-κB位点消除了在转染了HIV LTR指导细菌氯霉素乙酰转移酶基因表达的质粒的T细胞中TNF-α的激活作用。因此，TNF-α似乎通过诱导与HIV LTR中NF-κB序列结合的转录激活因子来激活ACH2细胞中的HIV RNA和病毒产生。
