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发表于 2002-8-24 21:15
J Hepatol 2002 Sep;37(3):355
肝脏杂志
Precore and core promoter mutations, hepatitis B virus DNA levels and
progressive liver injury in chronic hepatitis B.
前C/基本C区乙肝病毒变异, HBV DNA指数和肝脏损害
Yotsuyanagi H, Hino K, Tomita E, Toyoda J, Yasuda K, Iino S
Department of Internal Medicine, Division of Gastroenterology and
Hepatology, St. Marianna University School of Medicine, Miyamae-ku,
216-8512, Kawasaki, Japan
[Medline record in process]
BACKGROUND/AIMS: To elucidate the viral factors responsible for progressive liver injury in chronic hepatitis B.
背景/目标: 说明病毒是造成肝脏损害的因素
METHODS: We analyzed 179 persistently infected patients (21 asymptomatic carriers, 126 with chronic hepatitis and 32 with cirrhosis) with genotype C hepatitis B virus (HBV). HBeAg/anti-HBe, levels of HBV DNA, mutations in the basic core promoter (BCP) region at nucleotides 1762/1764 and mutation in the precore (preC) region at nucleotide 1896 were determined. Serial samples from 18 patients also were analyzed.
方法: 我们选择了179名"久治不愈"乙肝感染患者(21名无症状携带者, 126名慢性发言患者, 32名肝硬化患者), 他们都是携带乙肝病毒基因C型. HEeAg/anti_HBe, HBV DNA, 基本C区, 在1762/1764处, 变异(BCP), 前C区变异, 在1896处是观察的对象. 并对18为病人进行了系列取样分析.
RESULTS: HBeAg/anti-HBe and HBV DNA levels per se were not related to liver fibrosis. The frequency of BCP mutations increased with progression of liver fibrosis. Although the preC mutation was detected more often among the LC group, the role of this mutation in progression of fibrosis seems less than that of the BCP mutations. Sequential analysis showed that (1) rapidly progressing cases were positive continuously for double mutations in the BCP with a wild-type precore sequence, and (2) asymptomatic cases with anti-HBe acquired the preC mutation during their clinical course.
结果: HBeAg/anti-HBe 和 HBV DNA 含量与肝脏纤维化无关. 但是, BCP(基本C区变异)频lu的增加和肝脏纤维化进展成正比. 虽然前C区变异型病毒常常在肝癌族中发现, 但是它对于纤维化的影响似乎比基本C区变异要少. 系统分析说明(1)迅速恶化病例的增加在BCP双重变异并带有野生株前C区变异程序中是持续的; (2)无症状病例通常带有anti-HBe和前C区变异相关.
CONCLUSIONS: Double mutations in the BCP region at nucleotide
1762/1764 are closely related to progression of chronic liver disease.
Acquisition of mutation in the preC region at nucleotide 1896 may contribute to inactivation of chronic liver disease.
结论: 在基本C区(BCP)病毒的双重变异, 1762/1764处与慢性肝病的进展有关. 在前C区1896处的病毒变异可能是造成慢性肝病活动停止的因素.
PMID: 12175631, UI: 22166750
(仅供HBVHBV.COM网友内部交流, 指正)
[此贴子已经被liver411于2002-8-24 8:15:43编辑过]
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