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Early Evolution of Hepatitis C Virus (HCV) Quasispecies after Liver Transplant for HCV-Related Disease

Background. End-stage liver disease as a result of chronic hepatitis C virus (HCV) infection is the main indication for liver transplant (LT), but allografts are systematically infected with HCV soon after transplant. Viral quasispecies are poorly described during the early posttransplant period. Me...

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Bibliographic Details
Published in:The Journal of infectious diseases 2007-08, Vol.196 (4), p.528-536
Main Authors: Schvoerer, Evelyne, Soulier, Eric, Royer, Cathy, Renaudin, Anne-Catherine, Thumann, Christine, Fafi-Kremer, Samira, Brignon, Nicolas, Doridot, Stéphane, Meyer, Nicolas, Pinson, Patricia, Ellero, Bernard, Woehl-Jaegle, Marie-Lorraine, Meyer, Carole, Wolf, Philippe, Zachary, Pierre, Baumert, Thomas, Stoll-Keller, Françoise
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Language:English
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Summary:Background. End-stage liver disease as a result of chronic hepatitis C virus (HCV) infection is the main indication for liver transplant (LT), but allografts are systematically infected with HCV soon after transplant. Viral quasispecies are poorly described during the early posttransplant period. Methods. For 17 patients who received an LT for HCV disease, plasma viral quasispecies evolution was determined by sequence analysis of hypervariable region 1 of the E2 envelope gene before transplant (BT), after 7 days (D7), and after 1 month (M1). T helper (Th)1/Th2 cytokine levels were determined concomitantly. Results. HCV quasispecies showed a significant decrease in amino acid diversity at D7 and M1, compared with BT (P < .05). A correlation was observed between low plasma tumor necrosis factor-a levels at D7 and decreased quasispecies amino acid complexity at the same date. Nucleic acid diversity was lower for genotype 1 than for genotype 3 infection (P < .05). The complexity and diversity of amino acids were lower in patients with hepatocellular carcinoma (HCC) BT than in those without HCC (P < .05). Conserved amino acid residues within quasispecies were shared by the whole cohort before and after LT. Conclusion. Viral structural and/or host immunological features could favor the emergence of fitter HCV strains after LT.
ISSN:0022-1899
1537-6613
DOI:10.1086/519691