[韩国慢性乙型肝炎病毒感染患者前、核心启动子突变的患病率及临床意义]。

Hyung Joon Kim, Byung Chul Yoo
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引用次数: 0

摘要

背景/目的:韩国报道了乙型肝炎病毒(HBV)的前启动子和核心启动子突变,但其患病率和临床意义尚未确定。本研究的目的是确定韩国前核和核心启动子突变的患病率及其与乙型肝炎e抗原(HBeAg)状态、病毒复制水平和肝脏疾病严重程度的关系。方法:从1998年12月至1999年8月在中央大学附属医院肝病门诊就诊的患者中随机抽取150例:hbeag -DNA分支检测阳性患者50例,hbeag -DNA阴性患者50例,hbeag -DNA阴性患者50例。用聚合酶链反应(PCR)扩增这些患者的血清HBV- dna,并在135例HBV- dna阳性的患者中测定核心启动子/前核HBV序列。结果:135例HBV- dna序列均为含T核苷酸1858的HBV基因型。95.7%的hbeag阴性bdna阳性患者和94.9%的hbeag阴性bdna阴性患者检出前体细胞突变(A1896)。hbeag阳性患者88%为野生型,12%为野生型和A1896突变体的混合。hbeag阴性bdna阳性患者中93.5%、hbeag阴性bdna阴性患者中94.9%、hbeag阳性患者中74%检测到核心启动子TA突变(T1762/A1764)。未发现前核/核心启动子突变的存在与肝脏疾病严重程度或HBV-DNA水平之间存在相关性。结论:无论随后的病毒复制水平或疾病严重程度如何,HBeAg血清转换几乎总是发生前停止密码子突变。无论病毒复制水平或疾病严重程度如何,核心启动子TA突变在hbeag阳性患者和hbeag阴性患者中都很常见。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The prevalence and clinical significance of precore and core promoter mutations in Korean patients with chronic hepatitis B virus infection].

Background/aims: Precore and core promoter mutations of hepatitis B virus (HBV) have been reported in Korea but their prevalence and clinical significance have not been determined. The aims of this study were to determine the prevalence of precore and core promoter mutations and their relationships to hepatitis B e antigen (HBeAg) status, viral replication level, and severity of liver disease in Korea.

Methods: Among the patients who visited the Liver Diseases Clinics (Chung Ang University Hospital) between December 1998 and August 1999, 150 patients were randomly selected: 50 HBeAg-positive HBV-DNA positive patients by a branched DNA (bDNA) assay, 50 HBeAg-negative bDNA-positive patients, and 50 HBeAg-negative bDNA-negative patients. Serum HBV-DNA was amplified by a polymerase chain reaction (PCR) in these patients and the core promoter/precore HBV sequence was determined in 135 of the patients whose sera were positive for HBV-DNA by PCR.

Results: All of the 135 determined HBV-DNA sequences had HBV genotype with T at nucleotide 1858. Precore mutation (A1896) was detected in 95.7% of HBeAg-negative bDNA-positive patients and 94.9% of HBeAg-negative bDNA-negative patients. In HBeAg-positive patients 88% had wild type and 12% had mixture of wild type and A1896 mutant. Core promoter TA mutation (T1762/A1764) was detected in 93.5% of HBeAg-negative bDNA-positive patients, 94.9% of HBeAg-negative bDNA-negative patients and 74% of HBeAg-positive patients. No correlation was found between the presence of precore/core promoter mutations and liver disease severity or HBV-DNA levels.

Conclusion: Precore stop codon mutation occurred almost invariably, along with HBeAg seroconversion, irrespective of subsequent viral replication levels or disease severity. Core promoter TA mutation was frequent both in the HBeAg-positive patients and HBeAg-negative patients irrespective of viral replication levels or disease severity.

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