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目的 :研究乙型肝炎病毒 (HBV)C基因启动子 (CP)变异与无症状慢性HBV携带者 (AsC)肝炎发作及慢性乙肝病情严重性的关系。方法 :通过PCR及其产物直接测序 ,检测 4例AsC、2 7例慢性乙肝和 3例慢性重型乙肝病人血清的HBVCP和前C/C基因序列 ,并定量检测病人血清的HBVDNA。结果 :( 1)CP主要变异除核苷酸 (nt) 176 2 176 4双变异( 176 2A→T和 176 4G→A)外 ,还存在nt172 6 1730聚集变异 ( 172 6A→C、172 7A→T、1730C→G)。 ( 2 ) 11例首次急性发作的慢性乙肝病人中 (既往均有AsC史 ) ,8例出现CP聚集变异。而 5例隐匿起病的慢性乙肝病人和 4例AsC无一例出现该变异 ,且 1例在AsC状态时无CP变异 ,肝炎发作时出现CP聚集变异。 ( 3)CP聚集变异合并CP双变异的乙肝病人 ,临床上或表现为重型肝炎或迅速进展为活动性肝硬变 ,HBVDNA水平高滴度 ,HBVDNA(斑点法 )阳性 ,HBeAg/抗HBe转换。结论 :CP聚集变异与AsC肝炎急性发作有关 ;CP聚集变异与CP双变异同时存在 ,使慢性乙肝病人病情加重
Objective: To study the relationship between hepatitis B virus (HBV) C gene promoter (CP) mutation and the severity of asymptomatic chronic hepatitis B carriers (AsC) hepatitis and chronic hepatitis B (HBV). Methods: HBVCP and pre-C / C gene sequences were detected by PCR and direct sequencing of products in 4 AsCs, 27 chronic hepatitis B patients and 3 chronic severe hepatitis B patients. HBVDNA in serum of patients was detected quantitatively. Results: (1) In addition to the nucleotide variation (nt) 176 2 176 4 double mutation (176 2A → T and 176 4G → A), the main variation of CP was also found to be an aggregation mutation of nt172 6 1730 (172 6A → C, 172 7A → T, 1730C → G). (2) Of the 11 patients with chronic hepatitis B who had the first acute exacerbation (AsC history), 8 patients had CP aggregation variation. However, no mutation occurred in 5 patients with occult onset of chronic hepatitis B and 4 patients with AsC, and 1 patient had no CP mutation in AsC status and CP aggregation variation in hepatitis C attack. (3) Hepatitis B patients with CP aggregation mutation and CP double mutation were clinically or manifested as severe hepatitis or rapidly progressed to active cirrhosis with high titer of HBVDNA, positive HBVDNA (positive) and HBeAg / anti-HBe conversion. Conclusion: The variation of CP aggregation is related to the acute attack of AsC hepatitis. The aggregation of CP and CP double mutation coexist, which aggravates the chronic hepatitis B patients