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乙肝疫苗母-婴阻断失败者病毒全基因变异分析 总被引:3,自引:0,他引:3
Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants. 相似文献
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目的观察基于"伏邪"说的肝复安治疗慢性乙型病毒性肝炎(简称慢乙肝)患者铁代谢异常的临床疗效。方法将102例铁代谢异常相关性肝病(慢乙肝及肝硬化)患者分为治疗组(48例)与对照组(54例)。治疗组予中药"肝复安"辨证治疗,对照组予西医常规药物(抗病毒、保肝药)治疗。两组疗程均为36个月,观察肝脏铁质沉积疗效,比较血清铁代谢指标、肝功能、病毒及相关免疫指标等的变化情况。结果 1组间肝脏铁沉积疗效比较,第24个月、第36个月差异均有统计学意义,治疗组优于对照组(P0.05)。2组间治疗后比较,血清铁(SI)、血清铁蛋白(SF)浓度及异常率差异有统计学意义,治疗组较对照组降低程度更显著、指标异常率更低(P0.05)。组间治疗后比较,转铁蛋白(TRF)浓度及异常率差异有统计学意义,治疗组较对照组升高程度更显著、指标异常率更低(P0.05)。3组间治疗后比较,治疗组丙氨酸氨基转移酶(ALT)水平较对照组降低更为明显,差异有统计学意义(P0.05);乙肝表面抗原(HBs Ag)浓度差异有统计学意义,治疗组较对照组降低程度更显著(P0.05);CD3~+水平及异常率差异有统计学意义,治疗组较对照组升高程度更显著、指标异常率更低(P0.05);CD4~+/CD8~+异常率差异有统计学意义(P0.05)。结论基于"伏邪"说的肝复安治疗慢乙肝患者铁代谢异常,能有效纠正铁代谢异常,恢复免疫功能,抑制病毒复制,减轻肝脏损伤。 相似文献
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快速检测乙型肝炎病毒前核心区基因变异株方法的建立与初步应用 总被引:2,自引:0,他引:2
用聚合酶链反应(POR)选择性地扩增血清标本中乙型肝炎病毒(HBV)基因前C区(Pre-C)后,以三种寡核苷酸探针M0(野毒株基因序列)、M1(nt.1898位点突变株基因序列)、M2(nt.1998位及nt.1901位上双点突变株基因序列)在极其严谨的条件下分别杂交,检测EBVPre-C的最常见变异,结果本法具有根高的特异性。应用上述方法检测了31份乙肝病人的血清标本,结果7份HBeAg阳性标本中,有4份PCR阳性,均与M0探针杂交,未出现变异;24份抗-HBe阳性标本中,有10份PCR阳性,其中8份表现为M0伴M1和(或)M2阳性,一份为野毒株,另一份与三种探针均不杂交。 相似文献
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Objective To determine the factors responsible for failed postnatal immunoprophylaxis for hepatitis B virus(HBV) in Qidong, China. Methods Eleven children who developed into chronic HBV infection after receiving HBIG and HBV recombinant vaccines were recruited into the study. Eleven paired mothers with chronic hepatitis and other 6 mothers whose children successfully generated anti-HBs after im-munoprophylaxis were included as the control in the study. Full-length HBV DNA was amplified through ser-um sample by PCR method and underwent cloning and sequencing. HBV DNA level was quantified by real-time PCR. Results The mean levels of HBV DNA in mothers who had HBV DNA positive children and healthy children were ( 1.2 ×107± 3.1 × 106 ) copies/ml and ( 1.6× 107±8.8×106 ) copies/ml, respec-tively. There was no significant difference between the groups (P >0.05). Meanwhile, viral load in chil-dren was unrelated to that in their mothers (r2 =0.2429). In 11 HBV DNA positive children, 4(36.4% ) demonstrated amino acid substitutions in HBsAg "a" determinant region with 6 different types, I.e. T125A, I126T, Q129H, M133V, D144V and G145A. All of the mothers showed the wild-type sequence in "a" epitope, indicating surface escape mutants were not acquired from the initial infection, but developed under the immune pressure. The mutation rates after immunoprophylaxis for preS1, preS2, S, X, preC/C and P genes were 0.38%, 0. 22%, 0.27%, 0.17%, 0.11%, and 0.11%, respectively, nt2999-3157 in preS1, nt529-677 in S, nt1955-2016 in C, nt923-1001 and nt2489-2602 in P genes were among the hottest muta-tional spots throughout the HBV genome. Conclusion HBV mutation may occur in all the open readingframes after passive and active immunoprophylaxis. In addition to S gene, HBV preS and P genes could alsoassociate with the escape mutants. 相似文献
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乙型肝炎病毒X蛋白氨基端变异与肝癌发生的相关性分析 总被引:1,自引:0,他引:1
目的:探讨乙型肝炎病毒X蛋白(hepatitis B virus X protein, HBx)氨基端1~90位氨基酸(amino acid, AA)变异与肝细胞癌发生之间的关系.方法:采用PCR扩增产物直接测序的方法,对48例肝癌组织、159例肝癌和144例慢性肝炎患者血清中HBV X基因进行序列分析.通过病例-对照研究HBx变异与肝癌发生之间的关系.结果: 肝癌组织中HBx氨基端变异集中于1~49 AA区域,突变率为4.1%; 50~90 AA为保守区,突变率仅为0.46%. 血清检测结果显示,HBx氨基端突变在肝癌患者中的发生率显著高于肝炎患者(2.2% vs 1.8%,P<0.05); HBx第36位Ala/Thr/Pro→Ser的突变,在肝癌患者中的发生率为10.1%,显著高于肝炎患者中的2.1%[P<0.01,比数比(odds ratio,OR)=5.259, 95%可信区间为1.499~18.444)].A/T/P36S突变仅发生于C基因型病毒.结论:HBx 氨基端突变的累积可能与肝癌的发生有关.HBx A/T/P36S突变能增加C基因型HBV感染者发生肝癌的危险度. 相似文献
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目的:探讨血清中Glypican-3(GPC3)检测在肝癌诊断中的临床意义。方法:采用鼠抗GPC3(25-358aa)单克隆抗体和兔抗GPC3(379-393aa)多克隆抗体建立双抗夹心ELISA法,对364例原发性肝细胞肝癌、96例慢性乙型肝炎及106例正常人血清中GPC3进行定量。同时采用放射免疫法检测AFP。结果:原发性肝细胞肝癌患者血清GPC3平均浓度为86.96±422ng/mL;慢性乙型肝炎患者血清GPC3平均浓度为11.7±12.23 ng/mL;正常人血清GPC3平均浓度为6.04±9.21 ng/mL。原发性肝细胞肝癌患者血清GPC3含量与慢性乙型肝炎组和正常组比较差异显著(P<0.001),慢性乙型肝炎组和正常组间差异无统计学意义(P>0.05)。当以30 ng/mL为诊断界值时,GPC3诊断肝癌的敏感性和特异性分别为40%和93%。在151例同时检测AFP和GPC3的HCC血清中,AFP阳性率为49%,GPC3阳性率为40%。AFP联合GPC3检测时,能将HCC的检出率提高至72%。结论:血清GPC3可作为一新的肿瘤标志物用于原发性肝细胞肝癌的临床诊断。 相似文献
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[目的]探讨消化道印片细胞学镜下背景对恶性肿瘤诊断的临床意义。[方法]电子胃镜检查并取黏膜组织印片,作细胞学检查。[结果]消化道恶性肿瘤黏膜组织印片镜下背景可见癌性坏死,与炎性疾病时背景不同。[结论]消化道印片细胞学检查背景的分析判断有助于提高消化道恶性肿瘤的检查准确率,可以作为细胞学检查判断的一个指标。 相似文献
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肝癌中乙型肝炎病毒整合位点的分离鉴定 总被引:1,自引:0,他引:1
乙型肝炎病毒(HBV)慢性感染是导致肝癌发生的重要原因,HBV整合是致癌的可能机制之一。传统上,HBV整合位点的鉴定主要通过反复的筛选肝细胞癌(HCC)基因文库获得。现报道一种快速分离鉴定HBV整合位点的新方法,为探讨肝癌发生的分子机制提供新的研究手段。 相似文献