基础核心启动子突变的百分比对乙型肝炎e抗原血清转化后肝

StephenW

Impacts of the Percentage of Basal Core Promoter Mutation on the Progression of Liver Fibrosis After Hepatitis B e Antigen Seroconversion
Jia-Feng Wu, Kai-Chi Chang, Yen-Hsuan Ni, Hong-Yuan Hsu, Mei-Hwei Chang
The Journal of Infectious Diseases, Volume 223, Issue 8, 15 April 2021, Pages 1381–1389, https://doi.org/10.1093/infdis/jiaa545
Published:
29 August 2020
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Abstract
Background

We investigated the relationships among the percentage of hepatitis B virus (HBV) mutations and liver fibrosis after hepatitis B e antigen (HBeAg) seroconversion.
Methods

We quantified the percentage of HBV mutants by pyrosequencing using serum samples obtained at inflammatory phase and after HBeAg seroconversion in 160 initially HBeAg-positive chronic HBV-infected patients. The relationships between antiviral agents, percentages of HBV mutations, and liver stiffness measurements (LSMs) were analyzed.
Results

We demonstrated that the percentages of A1762T/G1764A mutation are significantly higher in subjects with an LSM >7 kPa than in those with an LSM ≤7 kPa after HBeAg seroconversion. Hepatitis B e antigen seroconversion age is positively correlated with the percentages of A1762T/G1764A mutation at inflammatory phase before HBeAg seroconversion. Subjects who underwent interferon, entecavir, or tenofovir disoproxil fumarate therapy before HBeAg seroconversion possessed a lower percentage of A1762T/G1764A mutation after HBeAg seroconversion. The percentage of A1762T/G1764A ≥20% after HBeAg seroconversion was predictive of an LSM >7 kPa (hazard ratio = 6.37, P = .001). The presence of A1762T/G1764A led to downregulated messenger ribonucleic acid and protein levels of programmed-death ligand-1 (PD-L1) in hepatocytes.
Conclusions

The percentage of A1762T/G1764A mutations after HBeAg seroconversion was associated with liver fibrosis. The A1762T/G1764A mutation may evoke hepatic inflammation by suppressing PD-L1 in hepatocytes.
antiviral agents, hepatitis B virus, liver stiffness measurement, transient elastography
Topic:

    mutation hepatic fibrosis antiviral agents hepatitis b e antigens interferons hepatitis b virus tenofovir entecavir human leukocyte interferon liver stiffness measurement programmed cell death 1 ligand 1 seroconversion

StephenW

基础核心启动子突变的百分比对乙型肝炎e抗原血清转化后肝纤维化进程的影响
吴家峰，张启智，倪仁H，徐洪元，张美慧
传染病杂志，2021年4月15日，第223卷，第8期，第1381-1389页，https：//doi.org/10.1093/infdis/jiaa545
发布时间：
2020年8月29日
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抽象的
背景

我们调查了乙型肝炎e抗原（HBeAg）血清转化后乙型肝炎病毒（HBV）突变百分比与肝纤维化之间的关系。
方法

我们使用在炎性期和HBeAg血清转化后在160名最初HBeAg阳性的慢性HBV感染患者中获得的血清样本，通过焦磷酸测序对HBV突变体的百分比进行了定量。分析了抗病毒药物，HBV突变百分比和肝硬度测量值（LSM）之间的关系。
结果

我们证明，HBeAg血清转化后，LSM> 7 kPa的受试者的A1762T / G1764A突变百分比显着高于LSM≤7 kPa的受试者。乙型肝炎e抗原血清转化年龄与HBeAg血清转化前炎症期A1762T / G1764A突变的百分比呈正相关。在HBeAg血清转化前接受干扰素，恩替卡韦或替诺福韦富马酸替诺福韦酯治疗的受试者在HBeAg血清转化后具有较低的A1762T / G1764A突变百分比。 HBeAg血清转化后A1762T / G1764A的百分比≥20％预测LSM> 7 kPa（危险比= 6.37，P = .001）。 A1762T / G1764A的存在导致肝细胞中信使核糖核酸和程序性死亡配体1（PD-L1）的蛋白质水平下调。
结论

HBeAg血清转化后A1762T / G1764A突变的百分比与肝纤维化有关。 A1762T / G1764A突变可通过抑制肝细胞中的PD-L1引起肝炎。
抗病毒药，乙型肝炎病毒，肝硬度测量，瞬时弹性成像
话题：

    突变肝纤维化抗病毒药乙型肝炎e抗原干扰素乙型肝炎病毒替诺福韦恩替卡韦人白细胞干扰素肝硬度测量程序性细胞死亡1配体1血清转化