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目的 探讨乙、丙型肝炎病毒（ＨＢＶ、ＨＣＶ） 重叠感染时，病毒之间的相互作用。方法 检测３０ 例ＨＢＶ、ＨＣＶ重叠感染患者血清病毒标志物的变化、ＨＢＶ前Ｃ区１ ８９６ 位点突变的发生比率及血清肿瘤坏死因子（ＴＮＦ）α、白细胞介素（ＩＬ）６ 含量。结果 与单纯ＨＢＶ或ＨＣＶ 感染者相比，重叠感染患者乙肝表面抗原（ＨＢｅＡｇ） 、ＨＢＶＤＮＡ、ＨＣＶＲＮＡ 阳性比率明显降低，乙肝ｅ 抗体（ 抗ＨＢｅ） 阳性比率明显升高，ＨＢｓＡｇ、抗ＨＢｃ ＩｇＧ 及抗ＨＣＶ 几何平均滴度也明显降低，部分患者ＨＢｓＡｇ 阴转。而ＨＢＶ前Ｃ区１ ８９６ 位点突变发生率及血清ＴＮＦα、ＩＬ６ 含量却明显高于单纯感染者。结论 ＨＢＶ、ＨＣＶ感染同一宿主时，存在相互干扰、抑制；ＨＢｅＡｇ 的消失、抗ＨＢｅ 的阳转既与ＨＣＶ对ＨＢＶ 复制的直接抑制有关，又与ＨＢＶ的前Ｃ区变异有关，且ＨＣＶ 的重叠感染可能是导致ＨＢＶ 前Ｃ区变异的原因之一，其作用机制可能与导致机体免疫压力升高有关
Objective To investigate the interaction between viruses when Hepatitis C and Hepatitis C virus (HBV, HCV) are over-infected. Methods The changes of serum viral markers and the incidence of mutation at 1896 sites in pre-HBV C and the levels of serum tumor necrosis factor (TNF) α and interleukin-6 were detected in 30 patients with HBV and HCV infection. Results The positive rates of HBeAg, HBVDNA and HCVRNA in patients with overlapping infection were significantly lower than those in patients with HBV or HCV infection alone, and the positive rates of anti- HBeAg and HBsAg were significantly higher Anti-HCV geometric mean titer was also significantly lower, some patients HBsAg negative. The pre-HBV C 1896 locus point mutations and serum TNFα, IL 6 levels were significantly higher than those infected alone. Conclusions HBV and HCV infection interfere with each other when they are infected with the same host. The disappearance of HBeAg and the anti-HBe activation are both related to the direct inhibition of HBV replication by HBV and the variation of pre-C region of HBV, and the overlap of HCV Infection may be one of the reasons leading to the variation of pre-HBV C region, and its mechanism may be related to the increase of immune pressure