Copeland K F
Centre for Molecular Medicine, Ottawa Hospital Research Institute, Ontario, Canada.
Arch Immunol Ther Exp (Warsz). 2001;49(1):13-8.
CD8+ T cells have been shown to produce factors which modulate HIV-1 replication in both T cells and monocytic cells. Examination of the literature reveals that this modulation may occur by the production of beta-chemokines which block viral entry. However, another CD8+ T cell-derived factor(s) targets the replication of HIV-1 at the level of transcription. CD8+ T cell factors strongly suppress replication at the level of transcription in T cells and T cell lines, the factors enhance both replication and transcription in cells of the monocyte/macrophage lineage. The enhancement of transcription and replication, which is pertussis toxin sensitive is induced by increased production of TNF-alpha by the target cells. Thus, CD8+ T cells produce factors which mediate effects on transcription and replication of HIV-1 in a cell type-dependent manner. In this review a summary of the effects of chemokines and CD8-derived factors on HIV-1 transcription and replication is presented focusing on the cellular pathways which may mediate their effects on HIV transcription and replication in different cell types. The virus-host cell interactions that participate in the persistent replication of HIV in macrophages and the suppression of these functions in T cells require definition. The identification of CD8+ T cell factors which exert these controls on HIV-1 may lead to promising new therapies for HIV infection.
CD8 + T细胞已被证明可产生调节HIV - 1在T细胞和单核细胞中复制的因子。查阅文献发现，这种调节可能是通过产生阻断病毒进入的β趋化因子来实现的。然而，另一种CD8 + T细胞衍生因子在转录水平靶向HIV - 1的复制。CD8 + T细胞因子在T细胞和T细胞系中强烈抑制转录水平的复制，而这些因子在单核细胞/巨噬细胞谱系的细胞中增强复制和转录。转录和复制的增强对百日咳毒素敏感，是由靶细胞中TNF -α产量增加诱导的。因此，CD8 + T细胞产生以细胞类型依赖性方式介导对HIV - 1转录和复制影响的因子。在这篇综述中，总结了趋化因子和CD8衍生因子对HIV - 1转录和复制的影响，重点关注可能介导它们对不同细胞类型中HIV转录和复制影响的细胞途径。参与HIV在巨噬细胞中持续复制以及在T细胞中这些功能抑制的病毒-宿主细胞相互作用需要明确。鉴定对HIV - 1发挥这些控制作用的CD8 + T细胞因子可能会带来有前景的HIV感染新疗法。
