乙型肝炎患者细胞免疫应答(CD8+CD38+)与乙型肝炎病毒DNA水平和HBsAg定量的关系

G. Shiha, E. Toson, A. Elbeeh, H. Abdellatif
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摘要

乙型肝炎病毒(HBV)感染是一个全球性的公共卫生问题。乙肝病毒的免疫应答是影响患者预后的一个关键因素。然而,病毒复制与宿主免疫反应性之间的关系仍是一个有待研究的问题。目的:本研究的目的是探讨新近诊断和治疗的初治慢性乙型肝炎(CHB)患者的细胞免疫应答是否可能受到HBV复制状态的影响。为此,研究HBV病毒载量、HBsAg定量与外周血t细胞亚群CD8+CD38+的相关性。方法:采用三色流式细胞术测定慢性乙型肝炎患者(50例)和健康对照(35例)CD8 - CD38 T细胞的比例和绝对计数。慢性乙型肝炎患者定期随访48周,在此期间每24个月检测T细胞亚群、血清病毒载量和HBsAg定量。结果:治疗前CD8+CD38+%水平(均值32.4514,标准差(SD) 16.8007)高于对照组(均值19.4628,SD 9.75555), p=0.000。与对照组(平均1944.13,SD 948.931)相比,HBV治疗开始12个月后CD8计数显著下降(平均1359.44,SD 724.362), p=0.001。CD8+CD38+计数与血清HBV DNA有显著相关性。CD8+CD38+计数与HBsAg定量呈正相关。结论:CD8+CD38+ T细胞与HBsAg含量呈正相关。在CHB患者中联合使用CD8+CD38+ T细胞、HBsAg定量和HBV DNA评估可以指导临床医生评估治疗反应的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cellular Immune Response (CD8+CD38+) in Relation to Hepatitis B Virus DNA Level and HBsAg Quantification in Hepatitis B Patients
Introduction: Hepatitis B Virus (HBV) infection is a global public health concern. The immune response in HBV represents a key factor in patient outcome. However, the relationship between viral replication and host immune reactivity remains a matter of investigation. Aim: The aim of our study was to investigate whether the cellular immune response of recently diagnosed and treatment naive chronic hepatitis B(CHB) patients may be influenced by the replicative status of HBV. Towards this aim, the correlation between HBV viral load, HBsAg quantification and peripheral T-cell subpopulations CD8+CD38+. Methods: Proportions and absolute counts of CD8 CD38 T cells were determined using three-color flow cytometry in chronic hepatitis B patients (n=50) and healthy controls (n=35). Chronic hepatitis B patients were regularly followed for 48 weeks, during which period the T cell subsets, serum viral load and HBsAg quantitation were measured every 24 months. Results: There was a high level of CD8+CD38+% during the pretreatment stage (Mean 32.4514, standard deviation (SD) 16.8007) compared to the control group (Mean 19.4628, SD 9.75555), p=0.000. Significant decreases in CD8 count were detected 12 months after treatment initiation of HBV therapy (Mean 1359.44, SD 724.362) compared to the control group (Mean 1944.13, SD 948.931), p=0.001. There is a significant correlation between CD8+CD38+ count and serum HBV DNA. A Positive correlation was found between CD8+CD38+ count and HBsAg quantitation. Conclusion: There was a positive correlation between CD8+CD38+ T cells and HBsAg quantitation. The combined use of CD8+CD38+ T cells, HBsAg quantitation and HBV DNA assessment in patients with CHB may guide the clinicians as they guage the likelihood of treatment response.
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