Down-regulation of human immunodeficiency virus type (HIV-1) production after stimulation of monocyte-derived macrophages infected with HIV-1.
Down-regulation of human immunodeficiency virus type (HIV-1) production after stimulation of monocyte-derived macrophages infected with HIV-1.
复制标题
刺激感染 HIV-1 的单核细胞来源的巨噬细胞后，人类免疫缺陷病毒型 (HIV-1) 的产生下调。
DOI：
--
复制
发表时间：
1993
影响因子：
6.4
通讯作者：
Jan Verhoef
中科院分区：
文献类型：
--
作者：
Hans S. L. M. Nottet;L. Graaf;N. M. Vos;Leendert J. Bakker;J. A. Strijp;Maarten R. Visser;Jan Verhoef
感染人类免疫缺陷病毒（HIV）的巨噬细胞会因继发感染而受到刺激。研究了刺激 HIV-1 感染的单核细胞来源的巨噬细胞对这些细胞产生 HIV-1 的影响。巨噬细胞暴露于佛波醇 12-肉豆蔻酸酯 13-乙酸酯或调理过的大肠杆菌、金黄色葡萄球菌或酵母聚糖会导致 HIV 产生减少。 HIV的产生与刺激程度成反比，刺激程度通过光泽精增强化学发光来测量。然而，活性氧中间体的产生似乎并不是艾滋病毒产生减少的直接原因，因为氧自由基清除剂并不能阻止艾滋病毒产生的减少。此外，氧自由基清除剂不影响未受刺激的巨噬细胞产生艾滋病毒。这些结果表明，与 T 细胞中描述的效果相比，激活信号具有相反的效果，并且活性氧中间体对巨噬细胞中 HIV 的产生没有影响。
Macrophages infected with human immunodeficiency virus (HIV) can be stimulated as a result of secondary infections. The effect of stimulation of HIV-1-infected monocyte-derived macrophages on HIV-1 production by these cells was studied. Exposure of macrophages to phorbol 12-myristate 13-acetate or to opsonized Escherichia coli, Staphylococcus aureus, or zymosan resulted in a decrease in HIV production. HIV production was inversely related to the degree of stimulation, measured as lucigenin-enhanced chemoluminescence. The production of reactive oxygen intermediates, however, did not seem to be the direct cause of the diminished HIV production, since oxygen-radical scavengers did not prevent the decrease in HIV production. Furthermore, oxygen-radical scavengers did not affect HIV production by nonstimulated macrophages. These results indicate that activation signals have an opposite effect and reactive oxygen intermediates have no effect on HIV production in macrophages compared with the effect described in T cells.