Laboratory of Stem Cell Biology, Divisions of Immunology, Cell and Molecular Biology, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, California 92121, USA.
Virology. 2010 Jun 5;401(2):131-6. doi: 10.1016/j.virol.2010.03.005. Epub 2010 Mar 24.
HIV-1 V3 loop clones of virus isolates derived from patients suffering from thrombocytopenia were used for infection of the human thymus/liver conjoint hematopoietic organ that developed in the severe combined immunodeficient mouse (SCID-hu Thy/Liv). The V3 loop clones showed a significantly greater degree of inhibition of megakaryopoiesis than myelopoiesis and erythropoiesis of the human CD34+ progenitor cells, in vivo. Inhibition of megakaryopoiesis occurs through reduction in c-Mpl expression and consequent decrease in STAT5 activation. Therefore HIV-1 V3 loop sequences of thrombocytopenic patients exhibit preferential inhibition of megakaryocyte lineage-specific differentiation of CD34+ progenitor cells, thus reflecting the patients' clinical condition.
从患有血小板减少症的患者中分离出的 HIV-1 V3 环病毒分离株的克隆被用于感染在严重联合免疫缺陷小鼠（SCID-hu Thy/Liv）中发育的人胸腺/肝联合造血器官。V3 环克隆在体内显著抑制巨核细胞生成的程度大于对人 CD34+祖细胞的骨髓生成和红细胞生成的抑制。巨核细胞生成的抑制是通过减少 c-Mpl 表达和随之而来的 STAT5 激活减少而发生的。因此，血小板减少症患者的 HIV-1 V3 环序列表现出对 CD34+祖细胞的巨核细胞谱系特异性分化的优先抑制，从而反映了患者的临床状况。
