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- W2053722322 abstract "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 (TH2)-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 TH1 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." @default.
- W2053722322 created "2016-06-24" @default.
- W2053722322 creator A5067004305 @default.
- W2053722322 date "2002-10-01" @default.
- W2053722322 modified "2023-09-30" @default.
- W2053722322 title "Pathogenesis of hepatitis C virus recurrence in the liver allograft" @default.
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- W2053722322 doi "https://doi.org/10.1053/jlts.2002.35856" @default.
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