Impact of hepatitis B virus infection on the activity of hematopoietic stem cell
- VernacularTitle:乙型肝炎病毒感染对造血干细胞活性的影响
- Author:
Yanmei SHI
;
Yinghua LAD
;
Lei SHAN
;
Huafeng CAI
;
Jingxia SUN
;
Yongchen WANG
;
Jin ZHOU
;
Yongguo LI
- Publication Type:Journal Article
- Keywords:
Hematopoietic stem cells;
Hepatitis B virus;
Dendritic cells;
Immunophenotyping
- From:
Chinese Journal of Infectious Diseases
2008;26(4):197-201
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the impact of hepatitis B virus (HBV) infection on the activity of cord hematopoietic stem cells. Methods CD34+ cells were isolated from healthy human cord blood by miniMACS. Cells were cultured in IMDM complete culture medium containing stem cell factor (SCF),fms-like tyrosine kinase 3 ligand (FL), thrombopoietin (TPO), interleukin-3 (IL-3) and 10% fetal bovine serum. High copies HBV were added to the culture system. The proliferation of stem ceils and virus replication were observed. Following the proliferation, dendritic cells (DCs) were induced by adding granulocyte-macrophage colony-stimulating factor and IL-4. Morphous of stem cells and DCs were observed by microscope and the cell surface molecules were detected. Results The proliferation of stem cells infected with HBV was significantly lower than that of healthy stem cells (P＜0.01),and enhanced after adding cytokines (P＜0.01). At the same time, HBV replication was increased after adding cytokines in the culture system (P＜0.01), but the proliferation was still lower than that of healthy stem cells with cytokines in the culture medium (P＜0.05). Dane particles were found in the cytoplasma of stem cells infected with HBV by electron microscope. The expression of CD80,CD86 ,CD1a and HLA-DR on DCs derived from HBV infected stem cells were all lower than those on DCs from non-infected stem cells (P＜0.01). Conclusions HBV could infect CD34+ stem cell and the proliferation of the stem cell could enhance the virus replication. HBV could not only inhibit the proliferation of stem cells,but also down-regulate the immuno-phenotype expression of DCs derived from CD34+stem cells.
