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Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
Hepatitis B virus reactivation is a risk factor for development of post-transplant lymphoproliferative disease after
Aibin Zhang1, Min Zhang, Yan Shen
1Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Abstract:
Post-transplant lymphoproliferative disease (PTLD) is believed to be associated with immunosuppressive regimens, underlying diseases and lymphotropic viral infections after organ transplantation. Hepatitis B virus (HBV) has been identified as a risk factor for non-Hodgkin's lymphoma, but no association between HBV and PTLD has been shown. In this study, we reviewed a series of 203 consecutive patients who underwent liver transplantation (LTx) for benign liver disease in our center. The patients comprised 144 patients with hepatitis B and 59 contemporary patients without hepatitis B. After LTx, 36 of the 144 patients with hepatitis B experienced HBV reactivation, while the remaining 108 patients did not. There was no difference in the incidences of PTLD between patients with and without hepatitis B (p = 0.497). Overall, four patients (11.1%) with HBV reactivation developed PTLD, compared to only one patient (0.9%) without HBV reactivation (p = 0.007). The relative odds for developing PTLD in patients with HBV reactivation were 17.5. No differences were observed for the follow-up periods, immunosuppressive regimens and rejection episodes (p > 0.05 for all). These data suggest that PTLD may be more prevalent in patients who experience HBV reactivation after liver transplantation. HBV reactivation may be a risk factor for development of PTLD.
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