title: Hepatitis B virus genotype G monoinfection and its transmission by blood components.
abstract: 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.
authors.affiliation: Paul-Ehrlich-Institut, Langen, Germany. chumi@pei.de
authors.forename: Michael
authors.initials: M
authors.lastname: Chudy
authors.forename: Michael
authors.initials: M
authors.lastname: Schmidt
authors.forename: Volker
authors.initials: V
authors.lastname: Czudai
authors.forename: Heinrich
authors.initials: H
authors.lastname: Scheiblauer
authors.forename: Sigrid
authors.initials: S
authors.lastname: Nick
authors.forename: Mira
authors.initials: M
authors.lastname: Mosebach
authors.forename: Michael Kai
authors.initials: MK
authors.lastname: Hourfar
authors.forename: Erhard
authors.initials: E
authors.lastname: Seifried
authors.forename: W Kurt
authors.initials: WK
authors.lastname: Roth
authors.forename: Elke
authors.initials: E
authors.lastname: Grünelt
authors.forename: C Micha
authors.initials: CM
authors.lastname: Nübling
mesh_terms: D000208:Acute Disease; D016913:Blood Component Transfusion / Q000009:adverse effects*; D004279:DNA, Viral / Q000235:genetics*; D005500:Follow-Up Studies; D005838:Genotype; D006509:Hepatitis B / Q000635:transmission* / Q000821:virology; D006514:Hepatitis B Surface Antigens / Q000276:immunology; D006515:Hepatitis B virus / Q000235:genetics* / Q000276:immunology / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012189:Retrospective Studies
chemical_list: D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens