BACKGROUND: Hepatitis C virus (HCV) infection is associated with the appearance of liver steatosis. AIM: To search for a correlation between the number of HCV infected hepatocytes and the presence, amount and distribution of steatosis. METHODS: A total of 124 frozen liver biopsies from HCV patients (genotype 3 = 21) were studied. HCV-antigens were detected on frozen liver sections using a four steps immunoperoxidase technique. Steatosis was graded by haematoxilin-eosin counterstaining on a serial section. RESULTS: Steatosis was detected in 82 of 124 (66.1%) patients without differences between different genotypes. Uric acid, body mass index, gammaGT levels significantly correlated with steatosis in non-3 (P < 0.01, P < 0.05, P < 0.01, respectively) but not in genotype 3 patients. HCV-antigens were detected in 95 of 124 (76.6%) cases. A positive correlation between steatosis and the number of infected hepatocytes was observed only in genotype 3 patients (P = 0.06). In most cases the number of cells with steatosis greatly outnumbered that of HCV infected cells. CONCLUSION: We confirm a possible role of the virus in the genesis of steatosis in HCV genotype 3 infected patients; however, as steatosis do not appear to be directly related to the presence of HCV-antigens within single hepatocytes, an indirect, possibly cytokine mediated, mechanism might be operative.
BACKGROUND:Hepatitis C virus (HCV) infection is associated with the appearance of liver steatosis. AIM: To search for a correlation between the number of HCV infected hepatocytes and the presence, amount and distribution of steatosis. METHODS: A total of 124 frozen liver biopsies from HCVpatients (genotype 3 = 21) were studied. HCV-antigens were detected on frozen liver sections using a four steps immunoperoxidase technique. Steatosis was graded by haematoxilin-eosin counterstaining on a serial section. RESULTS:Steatosis was detected in 82 of 124 (66.1%) patients without differences between different genotypes. Uric acid, body mass index, gammaGT levels significantly correlated with steatosis in non-3 (P < 0.01, P < 0.05, P < 0.01, respectively) but not in genotype 3 patients. HCV-antigens were detected in 95 of 124 (76.6%) cases. A positive correlation between steatosis and the number of infected hepatocytes was observed only in genotype 3 patients (P = 0.06). In most cases the number of cells with steatosis greatly outnumbered that of HCV infected cells. CONCLUSION: We confirm a possible role of the virus in the genesis of steatosis in HCV genotype 3 infected patients; however, as steatosis do not appear to be directly related to the presence of HCV-antigens within single hepatocytes, an indirect, possibly cytokine mediated, mechanism might be operative.
Authors: Richard K Sterling; Melissa J Contos; Paula G Smith; R Todd Stravitz; Velimir A Luketic; Michael Fuchs; Mitchell L Shiffman; Arun J Sanyal Journal: Hepatology Date: 2008-04 Impact factor: 17.425
Authors: Marion Depla; Louis d'Alteroche; Amélie Le Gouge; Alain Moreau; Christophe Hourioux; Jean-Christophe Meunier; Julien Gaillard; Anne de Muret; Yannick Bacq; Farhad Kazemi; Aurélie Avargues; Emmanuelle Roch; Eric Piver; Catherine Gaudy-Graffin; Bruno Giraudeau; Philippe Roingeard Journal: PLoS One Date: 2012-03-29 Impact factor: 3.240