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Medical Science Monitor Basic Research

AmJCaseRep
MedSciTechnol

eISSN: 2329-0358

Association of 49245A>G (rs868) Polymorphism in the 3’UTR of Donor TGFBR1 Gene with Course of Hepatitis C following Orthotopic Liver Transplantation

Bogna Ziarkiewicz-Wróblewska, Emir Sajjad, Michał Ciszek, Łukasz Hutnik, Dominika Łukasik, Mikołaj Fedorowicz, Tadeusz Wróblewski, Waldemar Patkowski, Leszek Pączek, Rafał Płoski, Paweł Włodarski, Jacek Malejczyk

Department of Pathology, Center for Biostructure Research, Medical University of Warsaw, Warsaw, Poland

Ann Transplant 2014; 19:643-651

DOI: 10.12659/AOT.891119

Available online: 2014-12-12

Published: 2014-12-12


#891119

Background: Terminal hepatitis C is one of the leading indications for orthotopic liver transplantation (OLT). However, hepatitis C virus (HCV) reinfection occurs in almost all recipients and usually leads to progressive fibrosis and graft failure. Transforming growth factor-b (TGF-β) plays a part in transplanted liver cirrhosis, but nothing is known about the possible role of genetic diversity of TGF-β receptor system. Therefore, the aim of our study was to investigate whether genetic variation in 3’ untranslated region (3’UTR) of TGF-β receptor type I (TGFBR1) gene is associated with recurrence and severity of hepatitis C and liver fibrosis following OLT in HCV-infected patients.
Material and Methods: The study group included 95 chronic hepatitis C patients following OLT. The recipients and donors were genotyped for 49245A>G (rs868) and 51976G>A (rs334349) single nucleotide polymorphisms (SNP).
Results: Donor rs868 AA genotype was strongly associated with worse clinical course of recurrent hepatitis C. The rs868 AA group displayed more severe symptoms of hepatitis C during the follow-up and the fibrosis score in this group was significantly higher 3 years after OLT.
Conclusions: Clinical course of hepatitis C after OLT may depend on donor rs868 SNP located in TGFBR1 3’UTR.

Keywords: Hepatitis C, Liver Transplantation, Polymorphism, Single Nucleotide



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