Harbol A W, Liesveld J L, Simpson-Haidaris P J, Abboud C N
Department of Medicine, University of Rochester School of Medicine, NY.
Blood Rev. 1994 Dec;8(4):241-51. doi: 10.1016/0268-960x(94)90112-0.
Human immunodeficiency virus (HIV) infection often has effects on the hematopoietic system which can be distinguished from the concurrent effects of medications or opportunistic infections. Exactly how the virus mediates these effects remains uncertain, but both in vivo and in vitro studies have pointed up possible direct and indirect modes of hematopoietic suppression. Whether a significant fraction of CD34+ cells in vivo are infected with HIV remains controversial, but most studies using in situ polymerase chain reaction techniques would suggest not. Other more indirect modes of hematopoietic cell suppression such as production of autoantibodies, production of other humoral inhibitory factors, T-cell mediated suppression of hematopoiesis, or production of inhibitory or stimulatory cytokines may also be contributory. It is probable that several of these mechanisms may occur simultaneously, and an increased understanding of their role may lead to improved strategies to correct the cytopenias which often accompany HIV disease.
人类免疫缺陷病毒（HIV）感染常常对造血系统产生影响，这种影响可与药物或机会性感染的并发影响区分开来。病毒究竟如何介导这些影响仍不确定，但体内和体外研究均指出了造血抑制的可能直接和间接模式。体内大部分CD34+细胞是否被HIV感染仍存在争议，但大多数使用原位聚合酶链反应技术的研究表明未被感染。造血细胞抑制的其他更间接模式，如自身抗体的产生、其他体液抑制因子的产生、T细胞介导的造血抑制或抑制性或刺激性细胞因子的产生，也可能起作用。这些机制中的几种可能同时发生，对其作用的进一步了解可能会带来改进策略，以纠正常伴随HIV疾病的血细胞减少症。
