In vitro hepatitis B virus infection of human bone marrow cells.

In vitro hepatitis B virus infection of human bone marrow cells.
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乙型肝炎病毒体外感染人骨髓细胞。

DOI:
10.1172/jci112591
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发表时间:
1986
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Gale,RP
Gale,RP
中科院分区:
--
文献类型:
--
作者:
Zeldis,JB;Mugishima,H;Steinberg,HN;Nir,E;Gale,RP

文献摘要

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人类感染B型肝炎病毒(HBV)经常导致造血抑制;在某些情况下,这可能导致严重的骨髓衰竭。HBV感染影响造血的机制尚不清楚。人骨髓体外暴露于HBV导致红系(红系爆发形成单位,BFU-E;红系集落形成单位CFU-E)、髓系(集落形成单位-粒细胞巨噬细胞CFU-GM)和淋巴(CFU-[T-淋巴细胞]-TL)造血干细胞的剂量依赖性抑制。灭活或免疫吸收血清中的HBV导致HBV诱导的造血干细胞抑制的损失。新生γ-干扰素在HBV感染骨髓细胞培养上清中未检出。γ干扰素抗体不影响HBV对造血干细胞的抑制。通过免疫电子显微镜在超过70%的未成熟造血细胞(包括成髓细胞、正常成粒细胞和成淋巴细胞)的细胞核中检测到B型肝炎表面抗原(HBsAg);粒细胞主要具有细胞质HBsAg。免疫过氧化物酶染色法也可在约5%的HBV感染骨髓细胞中检测到B型肝炎病毒核心抗原(HBcAg)。这些数据表明,HBV可以感染造血细胞和它们的祖细胞,从而表明HBV的嗜性范围比以前报道的更广。这些结果为HBV体外感染及HBV对造血的影响提供了实验依据。
Infection of humans with hepatitis B virus (HBV) frequently results in suppression of hematopoiesis; in some cases this may lead to severe bone marrow failure. The mechanism whereby HBV infection affects hematopoiesis is unknown. In vitro exposure of human bone marrow to HBV results in a dose-dependent inhibition of erythroid (erythroid burst forming units, BFU-E; erythroid colony-forming units CFU-E), myeloid (colony-forming units-granulocyte macrophage CFU-GM), and lymphoid (CFU-[T-lymphocytic]-TL) hematopoietic stem cells. Inactivation or immunoabsorption of HBV from sera resulted in loss of HBV-induced inhibition of hematopoietic stem cells. De novo gamma interferon was not detectable in the supernatants of cultures of bone marrow cells with HBV. Antibodies to gamma interferon did not affect the suppression of hematopoietic stem cells by HBV. Hepatitis B surface antigen (HBsAg) was detected by immune electron microscopy in nuclei of greater than 70% of immature hematopoietic cells including myeloblasts, normoblasts, and lymphoblasts; granulocytes had mostly cytoplasmic HBsAg. Hepatitis B virus core antigen (HBcAg) was also detected in about 5% of HBV infected bone marrow cells by immunoperoxidase staining. These data indicate that HBV can infect hematopoietic cells and their progenitors, thus suggesting a wider range of tropism for HBV than previously reported. These results may provide a basis to study HBV infection in vitro, and the effects of HBV on hematopoiesis.Images