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目的 研究乙型肝炎病毒 (HBV)C基因启动子 (CP)区域T176 2A176 4变异与慢性乙型肝炎病情严重性及干扰素应答的关系。方法 通过聚合酶链反应 (PCR)及其产物直接测序 ,检测 4例无症状慢性HBV携带者 (AsC)、2 7例慢性乙肝病人血清的HBVCP序列 ,并定量检测病人血清的HBVDNA水平。结果 CPT176 2A176 4变异在慢性乙肝病人的发生率为 5 1.9% ( 14 2 7) ,更多的是在病情较重 (肝损害中度以上 )的病例中出现 (P <0 .0 5 ) ,且该变异株具有生存优势。干扰素治疗 3个月后 ,感染该优势变异株的慢性乙肝病人血清HBVDNA拷贝数下降 36 .6± 2 5 .1倍 ,显著高于非变异株病人 ( 2 .5± 2 .1倍 ) ;HBeAg阴转率 ( 75 % )及HBVDNA(斑点法 )阴转率 ( 77.8% )也显著高于对照组 ( 16 .7% ,16 .7% ) ;对 4例变异干扰素组病人 3个月后再次测序 ,有 3例其变异株的生存优势被野生株 (WT)替代。结论 HBVCPT176 2A176 4变异株可能对干扰素较为敏感
Objective To study the relationship between the mutation of T176 2A176 4 in hepatitis C virus promoter (CP) region and the severity of chronic hepatitis B and the response to interferon. Methods HBVCP sequences in 4 asymptomatic chronic HBV carriers (AsC) and 27 chronic hepatitis B patients were detected by polymerase chain reaction (PCR) and direct sequencing of their products, and HBV DNA levels in serum of patients were detected quantitatively. Results The incidence of CPT176 2A176 4 mutation was 51.9% (14 2 7) in patients with chronic hepatitis B and more in those with severe disease (moderate liver damage) (P 0.05) And the mutant has survival advantage. After 3 months of interferon treatment, the serum HBVDNA copy number of chronic hepatitis B patients infected with this predominant variant decreased by 36.6 ± 2.51 times, significantly higher than that of non-mutant patients (2.5 ± 2.1 times). The negative conversion rates of HBeAg (75%) and HBVDNA (77.8%) were also significantly higher than those of the control group (16.7%, 16.7% After sequencing again, the survival advantage of 3 mutants was replaced by wild type (WT). Conclusion HBVCPT176 2A176 4 mutant may be more sensitive to interferon