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摘要: 目的探讨核苷类似物(NA)治疗达到完全应答(CR)的HBeAg阳性CHB患者与非活动性HBsAg携带者(IAgCs)之间HBV病毒学特点的异同。方法用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)以及部分PCR产物直接测序法对175例慢性HBV感染者进行HBV基因分型以及PC/BCP基因区变异检测,包括经NA治疗1年以上、达到CR的117例CHB患者(治疗组)和58例未行抗病毒治疗的IAgCs(对照组)。结果治疗组中1例A型、44例B型、16例C型,对照组中33例B型、10例C型、2例D型、1例基因型不明,两组的基因型构成比无统计学差异(P>0.05);治疗组BCP区A1762T/G1764A检出率显著低于对照组(9.8%vs 41.4%,P<0.01),PC区G1896A检出率亦明显低于对照组(14.0%vs 72.4%,P<0.01)。结论NA治疗达到CR的HBeAg阳性CHB患者PC/BCP变异检出率低于IAgCs。
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关键词:
- 肝炎病毒,乙型 /
- 非活动性HBsAg携带者 /
- 基因型 /
- 变异 /
- 核苷类似物
Abstract: Objective To investigate the virological differences between HBeAg positive hepatitis B patients with complete response to nucleot (s) ide anlogue treatment (NCRs) and inactive HBsAg carriers (IAgCs) .Methods HBV genotypes, A1896 and T1762/A1764 mutations were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in combination with direct nucleotide sequencing in a cohort of 175 patients with chronic HBV infection, including 117 patients with chronic hepatitis B (CHB) who had achieved completed response under the treatment of nucleot (s) ide analog (case group) , and 58 IAgCs who had achieved HBeAg seroconversion spontaneously (control group) .Results No statistical difference was found in the constituent ratio of HBV genotypes between these two groups (1 genotype A, 44 genotype B, 16 genotype C in the case group and 33 genotype B, 10 genotype C, 2 genotype D, 1 uncertain genotype in the control group;P>0.05) .Prevalence of A1762T/G1764A and G18896A were significantly lower in the case group (9.8% and 14.0%) than that in the control group (41.4% and 72.4%;both P<0.01) .Conclusion Prevalences of PC/BCP mutations of NCRs are lower than that of IAgCs.-
Key words:
- hepatitis B virus /
- lnactive HBsAg carrier /
- genotype /
- mutation /
- nucleot (s) ide analogue
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[1] 中华医学会肝病学分会, 感染病学分会.慢性乙型肝炎防治指南[J].中华肝脏病杂志, 2005, 13 (12) ∶881-891. [2]Schiff E R, Dienstag J L, Karayalcin S, et al.Lamivudine and 24weeks of lamivudine/interferon combination therapy for hepatitis B eantigen-positive chronic hepatitis B in interferon nonresponders[J].J Hepatol, 2003, 38 (6) ∶818-826. [3]王雪刚, 王战会, 马世武, 等.乙型肝炎病毒基因型及亚型与YM-DD、前C和C基因启动子变异的关系[J].肝脏, 2007, 13 (02) ∶95-98. [4]Chen C H, Lee C M, Lu S N, et al.Comparison of sequence chan-ges of precore and core promoter regions in HBeAg-positive chronichepatitis B patients with and without HBeAg clearance in lamivudinetherapy[J].J Hepatol, 2006, 44 (1) ∶76-82. [5]Cho S W, Hahm K B, Kim J H.Reversion from precore/core pro-moter mutants to wild-type hepatitis B virus during the course oflamivudine therapy[J].Hepatology, 2000, 32 (5) ∶1163-1169. [6]周彬, 黄月华, 单光华, 等.乙肝病毒基因型及病毒变异对慢性肝病进展的影响[J].热带医学杂志, 2008, 8 (04) ∶302-305. [7]Marrone A, Zampino R, Karayannis P, et al.Clinical reactivationduring lamivudine treatment correlates with mutations in the precore/core promoter and polymerase regions of hepatitis B virus in patientswith anti-hepatitis B e-positive chronic hepatitis[J].AlimentPharmacol Ther, 2005, 22 (8) ∶707-714. [8]Tong MJ, Blatt L M, Kao J H, et al.Basal core promoter T1762/A1764 and precore A1896 gene mutations in hepatitis B surface anti-gen-positive hepatocellular carcinoma:a comparison with chroniccarriers[J].Liver Int, 2007, 27 (10) ∶1356-1363. [9]Davis G L, Hoofnagle J H, Waggoner J G.Spontaneous reactivationof chronic hepatitis-B virus infection[J].Gastroenterology, 1984, 86 (2) ∶230-235.
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