Hepatitis B virus genotype G monoinfection and its transmission by blood components

Hepatitis B virus genotype G monoinfection and its transmission by blood components
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DOI:
10.1002/hep.21220
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发表时间:
2006-07-01
期刊:
影响因子:
13.5
通讯作者:
Nuebling, C. Micha
Nuebling, C. Micha
中科院分区:
医学1区
文献类型:
--
作者:
Chudy, Michael;Schmidt, Michael;Nuebling, C. Micha

文献摘要

被引文献

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通过乙肝表面抗原(HBsAg)检测和混合样本核酸扩增技术(NAT),在一名定期单采(血浆/血小板)捐献者中诊断出急性乙型肝炎病毒(HBV)感染。2周后通过检测抗 - HBc(IgM)和抗 - HBs确诊为急性感染。该捐献者无临床症状,丙氨酸氨基转移酶水平正常。他有每周捐献单采血浆或血小板的历史。作为回溯程序的一部分,使用灵敏的HBV NATs对捐献者的存档材料以及相应受血者进行了调查。在之前的捐献物以及两名输注血小板浓缩物的受血者中均可检测到HBV DNA。在所有HBV - DNA阳性样本中均鉴定出罕见的HBV G基因型。通过克隆测序、HBV基因型线性探针检测、基因型特异性NATs和限制性图谱分析,获得了G基因型单一感染的有力证据。与先前描述的均为与A基因型合并感染的G基因型感染不同,在任何样本中均未检测到乙肝e抗原(HBeAg)和抗 - HBe。这表明HBeAg对于病毒复制并非必需。在捐献者和受血者样本中检测HBsAg的延迟可能是由于在HBV感染早期G基因型特异性的不完全病毒形式合成减少,或者是当前HBsAg检测方法对G基因型的敏感性较低所致。总之,本次报告的HBV感染病例完全由G基因型引起。
An acute hepatitis B virus (HBV) infection was diagnosed in a regular apheresis (plasma/ platelet) donor by the hepatitis B surface antigen (HBsAg) assay and minipool nucleic acid amplification technology (NAT). The acute infection was confirmed by detection of anti-HBc (IgM) and anti-HBs 2 weeks later. The donor showed no clinical symptoms and had normal alanine aminotransferase levels. He had a history of weekly apheresis plasma or platelet donations. Archived material from the donor and the respective recipients was investigated by sensitive HBV NATs as part of a look-back procedure. HBV DNA was detectable in previous donations as well as in two recipients transfused with platelet concentrates. The rare HBV genotype G was identified in all HBV-DNA-positive samples. Strong evidence of genotype G monoinfection was obtained by clonal sequencing, HBV genotype line probe assay, genotype-specific NATs, and restriction pattern analysis. In contrast to previously described genotype G infections, which all appeared as coinfections with genotype A, neither the hepatitis B e antigen (HBeAg) nor anti-HBe was detectable in any of the samples. This shows that HBeAg is dispensable for viral replication. The delay in detecting HBsAg in both the donor and recipient samples may be explained by either decreased genotype G-specific synthesis of incomplete viral forms in early HBV infection or the lower sensitivity to genotype G of the current HBsAg assays. In conclusion, this reported case of an HBV infection was caused exclusively by genotype G.