首页> 中文期刊>河北医科大学学报 >乙型肝炎儿童T细胞亚群与病毒复制及病毒载量关系的研究

乙型肝炎儿童T细胞亚群与病毒复制及病毒载量关系的研究

     

摘要

目的 探讨乙型肝炎患儿T细胞亚群与病毒复制及病毒载量的关系.方法 选取乙型肝炎病毒脱氧核糖核酸(hepatitis B virus-desoxyribose nucleic acid,HBV-DNA)阳性的慢性乙型肝炎患儿58例为研究对象,其中乙型肝炎E抗原(human hepatitis B virus e antigen,HBeAg)阳性41例、HBeAg阴性17例,低载量患儿24例、中载量患儿19例、高载量患儿15例;另选取同期健康体检儿童35例为对照组.采用荧光定量PCR法检测HBV-DNA,应用流式细胞仪测定CD3+、CD4+、CD8+,计算CD4+/CD8+.结果 慢性乙型肝炎患儿CD3+、CD4+、CD4+/CD8+低于对照组,CD8+高于对照组(P<0.01).中载量组CD3+、CD4+、CD4+/CD8+低于低载量组,高载量组CD3+、CD4+、CD4+/CD8+低于低载量组和中载量组(P<0.01);中载量组和高载量组CD8+高于低载量组(P<0.01).HBeAg阳性患儿CD3+、CD4 +、CD4+/CD8+均低于HBeAg阴性患儿,CD8+高于HBeAg阴性患儿(P<0.01).结论 乙型肝炎患儿T细胞亚群的改变不仅与HBV感染有关,而且还与HBV-DNA复制有关,其复制可进一步加重细胞免疫功能紊乱.%Objective To explore the correlation of T lymphocytes with virus replication and viral load in children with hepatitis B.Methods Fifty-eight children with chronic hepatitis B,who were positive for hepatitis B virus-desoxyribose nucleic acid(HBV-DNA),were selected as the research subjects.Among them,41 had positive human hepatitis B virus e antigen(HBeAg),17 had negative HBeAg,24 had low viral load,19 had moderate viral load,and 15 had high viral load.Moreover,35 healthy children were served as the control group.FQ-PCR was used to detect HBV-DNA.FCM was used to detect CD3+,CD4+,and CD8+.CD4+/CD8+ were calculated.Results CD3+,CD4+,CD4+/CD8+ in children with Chronic hepatitis B were lower than the control group,CD8+ was higher than the control group (P<0.01).CD3+,CD4+,CD4+/CD8+ in load group were lower than that of low load group,CD3+,CD4+,CD4+/CD8+ in higher load group were lower than that of low load group and load group(P<0.01),load group and high load of CD8+ was higher than that of low load group(P<0.01).The CD3+,CD4+ and CD4+/CD8+ of HBeAg positive children were lower than those of HBeAg negative children,and CD8+ was higher than that of HBeAg negative children (P< 0.01).Conclusion Changes of T lymphocyte subsets in children with hepatitis B was not only associated with HBV infection,but also correlated with the replication of HBV-DNA,which can further aggravate the cellular immune dysfunction.

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