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Pathogenesis of hepatitis C virus recurrence in the liver allograft
Author(s) -
McCaughan Geoffrey W.,
Zekry Amany
Publication year - 2002
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2002.35856
Subject(s) - medicine , hepatitis c virus , immunology , pathogenesis , hepatitis c , liver transplantation , liver disease , virus , immune system , hepacivirus , virology , transplantation
1 Hepatitis C virus (HCV) infection in the allograft occurs in the setting of greater viral burden than in nontransplantation patients. 2 Infection of the allograft occurs early (within days and possibly during the intraoperative reperfusion phase). 3 Viral burden plateaus at 1 month posttransplantation and (in the absence of cholestatic HCV) peaks at the time of acute hepatitis (1 to 4 months). 4 Acute hepatitis is associated with immune cell infiltration and hepatocyte apoptosis. 5 Cholestatic HCV seems to be a disease of direct HCV cytopathic injury in the setting of extreme virus levels, an intrahepatic T helper subtype 2 cell (T H 2)‐like response, and lack of a specific HCV‐directed response. 6 Chronic hepatitic HCV seems to behave at the molecular and/or cellular level in a similar fashion to the nontransplantation setting, with activation of T H 1 inflammatory, profibrotic, and proapoptotic pathways. This process operates at a greater viral burden than pretransplantation and leads to more progressive disease. 7 More studies are required to examine and distinguish allograft rejection in the setting of HCV infection from HCV infection alone.