Ushijima H, Kunisada T, Ami Y, Tsuchie H, Takahashi I, Klöcking H P, Müller W E
Division of AIDS Virus, AIDS Research Center, National Institute of Health, Tokyo, Japan.
J Acquir Immune Defic Syndr (1988). 1992 Oct;5(10):1001-4.
The myeloid-monocytic cells ML-1, HL-60, THP-1, and U-937 were chronically infected (for > 2 years) with the lymphotropic human immunodeficiency virus type 1 (HIV-1) strain HTLV-IIIB. Reinfection experiments revealed that viruses obtained from chronically infected ML-1/HIV-1 and HL-60/HIV-1 cells showed a low infectivity if tested with uninfected ML-1 and HL-60 cells in contrast to virus preparations from chronically infected THP-1/HIV-1 and U-937/HIV-1 with their corresponding uninfected cell lines. Analyses of selected cell surface markers revealed a differential expression of CD4, CD8, CD11c, CD14, CD15, CD20, HLA-DR, and HLA-DQ in non- or chronically infected cells. In chronically infected cells, the steady-state levels for tumor necrosis factor-alpha, interleukin (IL)-1 beta, and granulocyte-macrophage colony-stimulating factor mRNA remained unchanged whereas the one for IL-6 dropped.
髓系单核细胞ML-1、HL-60、THP-1和U-937被嗜淋巴细胞的1型人类免疫缺陷病毒（HIV-1）毒株HTLV-IIIB长期感染（超过2年）。再感染实验表明，与来自慢性感染的THP-1/HIV-1和U-937/HIV-1及其相应未感染细胞系的病毒制剂相比，从慢性感染的ML-1/HIV-1和HL-60/HIV-1细胞中获得的病毒在用未感染的ML-1和HL-60细胞进行测试时显示出低感染性。对选定细胞表面标志物的分析显示，在未感染或慢性感染的细胞中，CD4、CD8、CD11c、CD14、CD15、CD20、HLA-DR和HLA-DQ存在差异表达。在慢性感染的细胞中，肿瘤坏死因子-α、白细胞介素（IL）-1β和粒细胞-巨噬细胞集落刺激因子mRNA的稳态水平保持不变，而IL-6的稳态水平下降。
