Busch F W, de Vos S, Flehmig B, Herrmann F, Sandler C, Vallbracht A
Med. Univ. Klinik Abt. II, Tübingen, Federal Republic of Germany.
Exp Hematol. 1987 Oct;15(9):978-82.
Inoculation of human bone marrow with hepatitis A virus (HAV) resulted in a dose- and duration-of-incubation-dependent suppression of hematopoietic progenitor (CFU-GM, BFU-E, CFU-Mix) growth in vitro. Monocytic progenitors appeared to be least affected. While HAV inactivation by heat or beta-propiolactone and neutralization by specific antibodies completely abrogated hematopoietic inhibition, depletion of adherent bone marrow cells, and enrichment of progenitors did not alter the pattern of suppression, which also seemed to be independent of HuIFN-alpha, -beta, -gamma, and TNF. These findings support the concept that direct infection of progenitor cells by HAV may be responsible for hematologic changes commonly seen during early phases of infectious hepatitis and possibly for some cases of bone marrow failure.
用人甲型肝炎病毒（HAV）接种人骨髓，在体外导致造血祖细胞（CFU-GM、BFU-E、CFU-Mix）生长受抑制，且这种抑制呈剂量和孵育时间依赖性。单核祖细胞似乎受影响最小。虽然通过加热或β-丙内酯使HAV灭活以及用特异性抗体中和可完全消除造血抑制，但去除贴壁骨髓细胞以及富集祖细胞并未改变抑制模式，而且这种抑制似乎也与HuIFN-α、-β、-γ和TNF无关。这些发现支持这样一种概念，即HAV对祖细胞的直接感染可能是传染性肝炎早期常见血液学改变的原因，也可能是某些骨髓衰竭病例的病因。
