von Laer D, Hufert F T, Fenner T E, Schwander S, Dietrich M, Schmitz H, Kern P
Clinical and Virological Department, Bernhard-Nocht Institute for Tropical Medicine, Hamburg, FRG.
Blood. 1990 Oct 1;76(7):1281-6.
Hematologic abnormalities occur in the majority of patients with acquired immunodeficiency syndrome (AIDS). Infection of the hematopoietic progenitor cells has been proposed as a potential explanation. In this study, different bone marrow cell populations, including the CD34+ hematopoietic progenitor cells, were purified by a fluorescence-activated cell sorter (FACS) and analyzed for the presence of human immunodeficiency virus-1 (HIV-1) proviral DNA using the polymerase chain reaction. A group of 14 patients with AIDS or AIDS-related complex (ARC) was studied (11 with peripheral blood cytopenias). The CD4+ helper cells in the bone marrow were found positive for HIV-1 DNA in all patients. In contrast, CD34+ progenitor cells were positive in only one patient. Two monocyte samples and two samples of CD4-/CD34- lymphocytes/blasts (mainly B and CD8 lymphocytes) were positive. Proviral DNA could not be detected in granulocytes. FACS analysis showed that the percentage of CD34+ hematopoietic progenitor cells was not altered in the bone marrow of AIDS patients in comparison with the HIV-1 seronegative controls. In contrast, the number of CD4+ lymphocytes was markedly reduced in the bone marrow of AIDS patients. These results show that the hematologic abnormalities in AIDS patients are neither explained by direct infection of the hematopoietic progenitor cells with HIV-1 nor by a depletion of progenitor cells.
大多数获得性免疫缺陷综合征(AIDS)患者会出现血液学异常。有人提出造血祖细胞感染是一种可能的解释。在本研究中,通过荧光激活细胞分选仪(FACS)纯化了包括CD34 +造血祖细胞在内的不同骨髓细胞群,并使用聚合酶链反应分析了人类免疫缺陷病毒1型(HIV-1)前病毒DNA的存在情况。研究了一组14例艾滋病或艾滋病相关综合征(ARC)患者(11例有外周血细胞减少)。所有患者骨髓中的CD4 +辅助细胞均被发现HIV-1 DNA呈阳性。相比之下,CD34 +祖细胞仅在一名患者中呈阳性。两份单核细胞样本以及两份CD4 - / CD34 -淋巴细胞/母细胞样本(主要是B淋巴细胞和CD8淋巴细胞)呈阳性。在粒细胞中未检测到前病毒DNA。FACS分析显示,与HIV-1血清阴性对照相比,艾滋病患者骨髓中CD34 +造血祖细胞的百分比没有改变。相反,艾滋病患者骨髓中CD4 +淋巴细胞的数量明显减少。这些结果表明,艾滋病患者的血液学异常既不能用HIV-1直接感染造血祖细胞来解释,也不能用祖细胞耗竭来解释。