HIV ENHANCER ACTIVITY PERPETUATED BY NF-KAPPA-B INDUCTION ON INFECTION OF MONOCYTES
HIV ENHANCER ACTIVITY PERPETUATED BY NF-KAPPA-B INDUCTION ON INFECTION OF MONOCYTES
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DOI：
10.1038/350709a0
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发表时间：
1991-04-25
期刊：
影响因子：
64.8
通讯作者：
VIRELIZIER, JL
中科院分区：
文献类型：
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作者：
BACHELERIE, F;ALCAMI, J;VIRELIZIER, JL
T淋巴细胞和巨噬细胞对人类免疫缺陷病毒(HIV)复制的容许性不同。在T细胞中，HIV转录在活体1中很少被检测到。克隆的正常T淋巴细胞显示出非常少的HIV增强子的基础活性和低核表达，NF-kappa-B2是HIV增强子3-5的有效转录激活剂。相比之下，固定的组织巨噬细胞表达可检测到的HIV蛋白，表明病毒永久转录6。巨噬细胞中病毒感染持续存在的一个解释可能是核内持续表达核转录因子-kappa-B。然而，完全允许HIV复制的U937单核细胞株仅表达低水平的核NF-kappa-B7。我们在这里表明，慢性HIV感染导致具有与NF-kappa-B没有区别的抗原性的核因子的诱导和永久性的HIV增强子活性增加。这一现象独立于肿瘤坏死因子，与艾滋病毒复制有关，因此可能至少部分解释了单核细胞中艾滋病毒感染的持久存在。
PERMISSIVENESS to replication of human immunodeficiency virus (HIV) differs in T lymphocytes and macrophages. In T cells, HIV transcription is poorly detected in vivo 1. Cloned, normal T lymphocytes show very little, if any, basal activity of the HIV enhancer and low nuclear expression of NF-kappa-B 2, a potent transcriptional activator of the HIV enhancer 3-5. In contrast, fixed tissue macrophages express detectable HIV proteins, indicating permanent virus transcription 6. One explanation for the perpetuation of virus infection in macrophages could be sustained nuclear NF-kappa-B expression. However, the U937 monocytic cell line, which is fully permissive to HIV replication, is known to express only low levels of nuclear NF-kappa-B 7. We show here that chronic HIV infection results in both induction of a nuclear factor with antigenic properties indistinguishable from those of NF-kappa-B and permanently increased HIV enhancer activity. This phenomenon, which is independent of tumour necrosis factor, is associated with HIV replication, and is thus likely to explain at least in part the perpetuation of HIV infection in monocytes.