Chai T, Prior S, Cooksley W G, Sing G K
Clinical Research Centre, Royal Brisbane Hospital Foundation, Australia.
J Infect Dis. 1994 Apr;169(4):871-4. doi: 10.1093/infdis/169.4.871.
Suspension cultures of bone marrow cells (BMC) were challenged with hepatitis B virus (HBV) to study interactions between the virus and the nonadherent and adherent BMC populations. Virus-challenged BMC developed an adherent stromal layer that differed in cellular composition from that of mock-infected cultures, showing a threefold increase in cells of the monocyte-macrophage lineage with an accompanying decrease in cells of the granulocytic lineage. Both viral envelope hepatitis B surface and core antigen expression was detected in adherent and nonadherent cell populations up to 10 days after virus challenge, which decreased thereafter. HBV DNA was still detectable in adherent cells 3 weeks after virus challenge, as shown by polymerase chain reaction analysis. These data indicate that HBV can infect not only bone marrow colony-forming cells but also the stromal cell populations involved with the regulation of hematopoiesis in vivo. Such virus-cell interactions could contribute to the immune dysfunction and bone marrow failure occasionally reported for patients with HBV infection as well as acting as an important site for HBV latency and persistence.
用乙型肝炎病毒（HBV）攻击骨髓细胞（BMC）的悬浮培养物，以研究病毒与非贴壁和贴壁BMC群体之间的相互作用。受病毒攻击的BMC形成了一层贴壁的基质层，其细胞组成与模拟感染培养物不同，单核细胞-巨噬细胞谱系的细胞增加了三倍，同时粒细胞谱系的细胞减少。在病毒攻击后长达10天的时间里，在贴壁和非贴壁细胞群体中均检测到病毒包膜乙型肝炎表面抗原和核心抗原的表达，此后表达下降。如聚合酶链反应分析所示，病毒攻击3周后，贴壁细胞中仍可检测到HBV DNA。这些数据表明，HBV不仅可以感染骨髓集落形成细胞，还可以感染体内参与造血调节的基质细胞群体。这种病毒-细胞相互作用可能导致HBV感染患者偶尔出现的免疫功能障碍和骨髓衰竭，并作为HBV潜伏和持续存在的重要部位。
