PATHOPHYSIOLOGICAL MECHANISMS OF HIV-INDUCED DEFECTS IN HEMATOPOIESIS - PATHOLOGY OF THE BONE-MARROW

被引:36
作者
STUTTE, HJ [1 ]
MULLER, H [1 ]
FALK, S [1 ]
SCHMIDTS, HL [1 ]
机构
[1] HOECHST AG,W-6230 FRANKFURT 80,GERMANY
来源
RESEARCH IN VIROLOGY | 1990年 / 141卷 / 02期
关键词
Pathophysiologie; VIH; Hématopoïèse; Moelle osseuse; SIDA;
D O I
10.1016/0923-2516(90)90021-A
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Bone marrow biopsies of 96 HIV1-infected patients were analysed histologically and by immuno- and enzyme histochemical techniques. Independently of the stage of disease, the bone marrow frequently exhibits hypercellularity and features of dysplastic haemopoiesis combined with mesenchymal alterations. In situ immunohistochemical analysis shows that there is a marked reduction in expression of the proliferation-associated nuclear antigen recognized by the Ki67 antibody. Comparison with non-infected controls reveals that there is a reduction in CD34+/myeloperoxidase-/naphthol AS-D chloroacetate- progenitor cells and an overproportional decrease in CD8+ lymphocytes in the bone marrow. Double staining revealed the presence of gag-coded HIV1 proteins in the above-mentioned CD34+ progenitor cells, in myelopoiesis cells, megakaryocytes and above all, in CD68+/acid phosphatase+ and alkaline phosphatase+ bone marrow reticular cells. From the latter results, it was concluded that HIV1-infected reticular cells may be disturbed in their ability to produce factors responsible for the short-range regulation of haemopoietic activity. © 1990.
引用
收藏
页码:195 / 200
页数:6
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