Wietzke P, Schott P, Braun F, Mihm S, Ramadori G
Department of Medicine, Division of Gastroenterology and Endocrinology, Georg-August-Universität, Göttingen, Germany.
Liver. 1999 Aug;19(4):348-53. doi: 10.1111/j.1478-3231.1999.tb00060.x.
The routes of hepatitis B virus and hepatitis C virus transmission are quite similar and coexistence of both viruses in one patient is not a rare phenomenon. Until now, the natural course of liver diseases induced by coinfections has not been well documented and the mechanisms of interaction between the two viruses and the human host have not been fully clarified. We report the case of a patient suffering from chronic hepatitis due to hepatitis C virus who developed an acute hepatitis B virus superinfection. Serum hepatitis C virus ribonucleic acid became undetectable by reverse transcriptase/polymerase chain reaction at diagnosis of acute hepatitis B virus infection. At the same time, there was a striking increase in the serum concentrations of the antibodies against C22 and C33c hepatitis C virus antigens. Four months after clinical resolution of the acute hepatitis, hepatitis B surface antigen was undetectable in serum and three months later antibodies against hepatitis B surface antigen appeared. Two years after acute hepatitis B virus infection, the patient has had no relapse of markers for viral replication of hepatitis B virus. Transaminases are within the reference range and hepatitis C virus ribonucleic acid is undetectable in both serum and liver tissue. We hypothesize that acute hepatitis B virus infection stimulated a specific humoral response against hepatitis C virus as well as triggering non-specific defense mechanisms which finally eliminated both viruses.
乙型肝炎病毒和丙型肝炎病毒的传播途径颇为相似，两种病毒在同一患者体内共存并非罕见现象。迄今为止，合并感染所致肝脏疾病的自然病程尚无充分记录，两种病毒与人类宿主之间的相互作用机制也未完全阐明。我们报告了一例因丙型肝炎病毒导致慢性肝炎的患者，其发生了急性乙型肝炎病毒重叠感染。在诊断急性乙型肝炎病毒感染时，通过逆转录/聚合酶链反应检测不到血清丙型肝炎病毒核糖核酸。与此同时，针对丙型肝炎病毒C22和C33c抗原的抗体血清浓度显著升高。急性肝炎临床缓解四个月后，血清中检测不到乙型肝炎表面抗原，三个月后出现了针对乙型肝炎表面抗原的抗体。急性乙型肝炎病毒感染两年后，患者乙型肝炎病毒复制标志物未复发。转氨酶在参考范围内，血清和肝组织中均检测不到丙型肝炎病毒核糖核酸。我们推测，急性乙型肝炎病毒感染激发了针对丙型肝炎病毒的特异性体液反应，并触发了非特异性防御机制，最终清除了两种病毒。
