Reactivation of hepatitis B virus with mutated hepatitis B surface antigen in a liver transplant recipient receiving a graft from an antibody to hepatitis B surface antigen- and antibody to hepatitis B core antigen-positive donor.

TitleReactivation of hepatitis B virus with mutated hepatitis B surface antigen in a liver transplant recipient receiving a graft from an antibody to hepatitis B surface antigen- and antibody to hepatitis B core antigen-positive donor.
Publication TypeJournal Article
Year of Publication2012
AuthorsBlaich A, Manz M, Dumoulin A, Schuttler CG, Hirsch HH, Gerlich WH, Frei R
JournalTransfusion// // Transfusion
Volume52
Issue9
Pagination1999 - 2006
Date Published2012//
ISBN Number1537-2995
Other Numberswdn, 0417360
Keywords*Hepatitis B Antibodies/bl [Blood], *Hepatitis B Surface Antigens/ge [Genetics], *Hepatitis B virus/ph [Physiology], *Hepatitis B/tm [Transmission], *Liver Transplantation/ae [Adverse Effects], *Virus Activation/ph [Physiology], Hepatitis B Core Antigens/im [Immunology], Hepatitis B Surface Antigens/im [Immunology], Hepatitis B virus/ge [Genetics], Hepatitis B virus/im [Immunology], Hepatitis B/bl [Blood], Hepatitis B/et [Etiology], Hepatitis B/vi [Virology], Humans, Male, Middle Aged, Mutation/ph [Physiology], Tissue Donors
Abstract

BACKGROUND: Fresh-frozen plasma (FFP) may contain antibodies to hepatitis B surface antigen (HBsAg, anti-HBs). These anti-HBs may lead to a misinterpretation of the actual hepatitis B immune status. Furthermore, they may not only confer protection against hepatitis B virus (HBV), but may also favor the selection of HBsAg mutants., CASE REPORT: We report a case of de novo HBV infection in a HBV-naive recipient with alcoholic liver disease, who received a liver from a donor with antibodies to hepatitis B core antigen (HBcAg, anti-HBc) and anti-HBs., RESULTS: A lookback investigation revealed the following: 1) Due to anti-HBs passively acquired through FFP, the recipient was considered immune to HBV and did not receive anti-HBV prophylaxis. 2) Within 1 year after transplantation he developed hepatitis B in absence of any elevated liver enzymes after the anti-HBs by FFP declined. 3) Despite an infection with HBV-containing wild-type HBcAg, the patient did not seroconvert to anti-HBc positivity. 4) The replicating HBV encoded two HBsAg mutations, first sQ129R and 4 months later sP127S. They map to the highly conserved "alpha" determinant of the HBsAg loop., CONCLUSION: 1) Passive transfer of anti-HBs from FFP led to an erroneous pretransplant diagnosis of HBV immunity when the patient was in fact HBV-naive. 2) HBsAg mutations might have been selected in escape from donor's actively produced anti-HBs and the recipient's anti-HBs by FFP might have favored this selection. 3) It is doubtful whether hepatitis B immunoglobulin could have prevented the reactivation. 4) Antiviral prophylaxis would have been crucial.Copyright © 2012 American Association of Blood Banks.

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