Allain J-P
Division of Transfusion Medicine, Department of Haematology, University of Cambridge, Cambridge, UK.
Vox Sang. 2004 Feb;86(2):83-91. doi: 10.1111/j.0042-9007.2004.00406.x.
Hepatitis B virus (HBV) presents a higher residual risk of transmission by transfusion than hepatitis C virus (HCV) or human immunodeficiency virus (HIV). While most infectious blood units are removed by screening for hepatitis B surface antigen (HBsAg), there is clear evidence that transmission by HBsAg-negative components occurs, in part, during the serologically negative window period, but more so during the late stages of infection. Donations negative for HBsAg, but positive for HBV DNA, with or without the presence of HBV antibodies, correspond to 'occult' HBV infection (OBI). The frequency of OBI depends on the relative sensitivity of both HBsAg and HBV DNA assays. It also depends on the prevalence of HBV infection in the population. OBI may follow recovery from infection, displaying antibody to hepatitis B surface antigen (anti-HBs) and persistent low-level viraemia, escape mutants undetected by the HBsAg assays, or healthy carriage with antibodies to hepatitis B e antigen (anti-HBe) and to hepatitis B core antigen (anti-HBc). Over time, in the latter situation, anti-HBe and, later, anti-HBc may become undetectable. The critical question is whether or not OBI is infectious by transfusion. All forms have been shown to be infectious in immunocompromised individuals, such as organ- or bone marrow-transplant recipients. In immunocompetent recipients, there is no evidence that anti-HBs-containing components (even at low titre) are infectious. Anti-HBc only, with HBV DNA, can be associated with infectivity, as can rare cases of HBV DNA without any serological HBV marker. If HBV nucleic acid amplification technology (NAT) is considered, the OBI viral load would usually be < 500 IU/ml, making testing of plasma pools unsuitable unless the sensitivity of NAT significantly increases by genome enrichment or test improvement.
与丙型肝炎病毒（HCV）或人类免疫缺陷病毒（HIV）相比，乙型肝炎病毒（HBV）经输血传播的残余风险更高。虽然大多数具有传染性的血液单位通过筛查乙型肝炎表面抗原（HBsAg）被剔除，但有明确证据表明，HBsAg阴性成分的传播部分发生在血清学阴性窗口期，但在感染后期更为常见。HBsAg阴性但HBV DNA阳性（无论是否存在HBV抗体）的献血对应于“隐匿性”HBV感染（OBI）。OBI的发生率取决于HBsAg和HBV DNA检测的相对灵敏度。它还取决于人群中HBV感染的流行率。OBI可能发生在感染恢复后，表现为具有乙型肝炎表面抗原抗体（抗-HBs）和持续低水平病毒血症，可能是HBsAg检测未发现的逃逸突变株，或者是携带乙型肝炎e抗原抗体（抗-HBe）和乙型肝炎核心抗原抗体（抗-HBc）的健康携带者。随着时间的推移，在后一种情况下，抗-HBe以及随后的抗-HBc可能会变得检测不到。关键问题是OBI是否具有输血传染性。所有形式的OBI在免疫功能低下的个体（如器官或骨髓移植受者）中都已被证明具有传染性。在免疫功能正常的受者中，没有证据表明含有抗-HBs的成分（即使滴度很低）具有传染性。仅抗-HBc与HBV DNA同时存在时可能与传染性有关，没有任何血清学HBV标志物的罕见HBV DNA病例也可能具有传染性。如果考虑使用HBV核酸扩增技术（NAT），OBI的病毒载量通常会<500 IU/ml，除非通过基因组富集或检测改进显著提高NAT的灵敏度，否则对血浆池进行检测并不合适。
