BMC Infect Dis. 2013 May 16;13:223. doi: 10.1186/1471-2334-13-223.
About ninety percent of immunocompetent adults recover from hepatitis B virus (HBV) infection within 6 months after transmission. The infection is considered to be terminated if the antibodies (HBsAb) to the hepatitis B surface antigen (HBsAg) become detectable and the HBsAg and Hepatitis B virus DNA (HBV DNA,) are no longer perceptible. After recovery from an acute infection, the detection of HBsAb is assumed to indicate lifelong immunity. However, after initiation of severe immunosuppression, HBV reactivation, as detected by HBsAg seroreversion may be observed in patients with previously resolved HBV infections.
We present an unusual case of a 64-year-old Caucasian woman showing clinically apparent HBV seroreversion more than 45 months after hematopoietic stem cell transplantation (HSCT). Despite living without immunosuppressive agents for more than 40 months, she developed a fulminant HBV infection with detection of a mutated hepatitis B virus carrying two immune escape mutations (D144E/G145R) in the HBsAg (HBsIE mutation).
After HSCT, the absence of risk factors such as strong immunosuppression and graft-versus-host disease decreases the risk of HBV seroreversion but may rearward seroreversion to a later time. Therefore, when monitoring HSCT, patients with serological markers of a resolved HBV infection [HBcAb + (hepatitis B core antibody), HBsAb+, and HBsAg-], the follow up has to be extended over several years to exclude HBV reactivation with HBsAg seroreversion. Furthermore, this case demonstrates the complexity of virus evolution after HBsAg seroreversion as a result of immunosuppression after HSCT.
约 90%的免疫功能正常成年人在感染乙型肝炎病毒 (HBV) 后 6 个月内从感染中恢复。如果检测到乙型肝炎表面抗原 (HBsAg) 的抗体 (HBsAb) 并检测不到 HBsAg 和乙型肝炎病毒 DNA (HBV DNA)，则认为感染已终止。急性感染后恢复，检测到 HBsAb 被认为可提供终身免疫。然而，在开始严重免疫抑制后，以前已解决的 HBV 感染患者可能会观察到 HBsAg 血清学转换导致的 HBV 再激活。
我们报告了一例不寻常的病例，一名 64 岁白人女性在造血干细胞移植 (HSCT) 后 45 个月以上表现出明显的 HBV 血清学转换。尽管她在没有免疫抑制剂的情况下生活了超过 40 个月，但她发生了暴发性 HBV 感染，在 HBsAg 中检测到携带两种免疫逃逸突变 (D144E/G145R) 的突变乙型肝炎病毒 (HBsIE 突变)。
在 HSCT 后，缺乏强免疫抑制和移植物抗宿主病等危险因素会降低 HBV 血清学转换的风险，但可能会将血清学转换延迟到更晚的时间。因此，在监测 HSCT 时，对于具有 HBV 感染已解决血清学标志物（HBcAb +（乙型肝炎核心抗体）、HBsAb+和 HBsAg-）的患者，随访时间必须延长数年，以排除 HBsAg 血清学转换的 HBV 再激活。此外，本病例表明，在 HSCT 后免疫抑制导致 HBsAg 血清学转换后，病毒进化的复杂性。
