The prevalence of hepatitis B virus preS deletions occurring naturally in Korean patients infected chronically with genotype C
The prevalence of hepatitis B virus preS deletions occurring naturally in Korean patients infected chronically with genotype C
复制标题
DOI：
10.1002/jmv.21208
复制
发表时间：
2008-07-01
影响因子：
12.7
通讯作者：
Kim, Bum-Joon
中科院分区：
文献类型：
--
作者：
Mun, Ho-Suk;Lee, Seoung-Ae;Kim, Bum-Joon
虽然韩国是B型肝炎病毒感染（HBV）的流行地区之一，但HBV前S区天然缺失的流行率尚未确定。在本研究中，根据临床状态和HBeAg血清学状态确定了120例具有不同临床特征的患者[59例HBeAg阳性，61例HBeAg阴性; 38例无症状携带者，21例慢性肝炎患者，21例肝硬化患者，40例肝细胞癌（HCC）患者]中preS缺失的患病率。共有37株（30.8%）在preS区域中具有缺失。总体而言，preS缺失的频率倾向于根据肝脏疾病的临床严重程度逐渐增加。肝癌患者中preS 1缺失的发生率倾向于高于肝硬化患者（32.5% vs. 19%）。HBeAg阴性患者中preS 2缺失的发生率显著高于HBeAg阳性患者（23% vs. 6.8%）。最常见的缺失类型是破坏preS 1起始密码子[14/37株（37.8%）]，这在HCC患者中显示出非常高的患病率（9/40，22.5%; HCC与无症状携带者，P=0.048）。提示preS 1和preS 2基因突变在促进慢性肝病尤其是肝癌的进展和维持免疫耐受阶段的耐受机制上可能存在差异。破坏preSi起始密码子类型的特异性缺失可能在肝癌发生中发挥重要作用，至少在患有慢性HBV感染的韩国患者中是这样。
Although Korea is one of the endemic areas for hepatitis B virus infection (HBV), the prevalence of deletions in HBV preS region occurring naturally have not been determined. In the present study, the prevalence of preS deletions was determined in terms of clinical state and HBeAg serostatus in 120 patients with different clinical features [59 HBeAg positive, 61 HBeAg negative; 38 asymptomatic carriers, 21 patients with chronic hepatitis, 21 patients with liver cirrhosis, 40 patients with hepatocellular carcinoma (HCC)]. A total of 37 strains (30.8%) harbored deletions in the preS region. Overall, the frequencies of preS deletions tended to increase gradually according to the degree of the clinical severity of liver disease. The prevalence of preS1 deletions in HCC patients tended to be higher than in patients with liver cirrhosis (32.5% vs. 19%). The prevalence of preS2 deletions in HBeAg negative patients was significantly higher than in HBeAg positive patients (23% vs. 6.8%). The type of deletion encountered most frequently was one disrupting the preS1 start codon [14/37 strains (37.8%)], which showed a very high prevalence in HCC patients (9/40, 22.5%; HCC vs. asymptomatic carriers, P=0.048). These results suggest that there might be the discrepancy between preS1 and preS2 mutations in the mechanism of enhancing the progression of chronic liver disease, especially the development of HCC and to maintain tolerance during the stage of immune tolerance. Specific deletion of the type disrupting preSi start codon may play important roles in hepatocarcinogenesis, at least in Korean patients with chronic HBV infection.