Human immunodeficiency virus causes mononuclear phagocyte dysfunction.
Human immunodeficiency virus causes mononuclear phagocyte dysfunction.
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人类免疫缺陷病毒会导致单核吞噬细胞功能障碍。
DOI：
10.1073/pnas.87.10.3933
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发表时间：
1990
影响因子：
11.1
通讯作者：
Golde,DW
中科院分区：
文献类型：
--
作者：
Baldwin,GC;Fleischmann,J;Chung,Y;Koyanagi,Y;Chen,IS;Golde,DW
有令人信服的临床证据表明，艾滋病患者的单核巨噬细胞系统功能障碍，这被认为部分是由于T细胞合作能力的丧失。人类免疫缺陷病毒感染对巨噬细胞功能的直接影响尚不清楚。为了解决这个问题，我们在体外用一种嗜单核细胞的人类免疫缺陷病毒株感染了正常的人巨噬细胞，并进行了细胞外和细胞内杀伤能力的测定。人类免疫缺陷病毒感染的巨噬细胞在介导抗体依赖细胞介导的针对白血病细胞靶点的细胞毒作用和假热带念珠菌的细胞内杀伤方面明显低于对照细胞。这些功能缺陷是严重的，暂时与巨噬细胞活跃的病毒产生有关，粒细胞-巨噬细胞集落刺激因子无法克服。感染后6天用3‘-叠氮-3’-脱氧胸腺嘧啶核苷(AZT)处理巨噬细胞，可显著降低病毒产量，阻止细胞内杀伤功能缺陷的发生。结果表明，早期抗病毒治疗可能有助于预防或缓解病毒诱导的单核细胞吞噬功能障碍。
There is compelling clinical evidence for dysfunction of the mononuclear phagocyte system in patients with AIDS, which is believed due in part to loss of T-cell cooperativity. The direct consequences of human immunodeficiency virus infection on macrophage function are unknown. To address this question we infected normal human macrophages in vitro with a monocytotropic strain of human immunodeficiency virus and performed assays to quantify their extra- and intracellular killing ability. Human immunodeficiency virus-infected macrophages were significantly less effective than control cells in mediating antibody-dependent cell-mediated cytotoxicity against leukemic cell targets and intracellular killing of Candida pseudotropicalis. The functional defects were profound, related temporarily to active virus production by the macrophages, and could not be overcome by granulocyte-macrophage colony-stimulating factor. Treatment of macrophages with 3'-azido-3'-deoxythymidine (AZT) 6 days after infection caused a marked decrease in virus production and prevented development of the intracellular killing functional defect. The results suggest that early antiviral therapy may be useful in preventing or mitigating some virus-induced mononuclear phagocyte dysfunction.