Hepatocyte steatosis is a cytopathic effect of hepatitis C virus genotype 3.
By L. Rubbia-Brandt, R. Quadri, K. Abid, E. Giostra, P. Male, Gilles Mentha, L. Spahr, J. Zarski, B. Borisch, A. Hadengue and 1 more. Journal of Hepatology, 2000
610 citations recorded by the source corpus.
Subfields: Emergency Medicine, Epidemiology, Hepatology
View Paper: https://www.semanticscholar.org/paper/a08f714ce3184226f4f0ae8696886b5e5e4cf972
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Citations in the corpus
- Effect of treatment with peginterferon or interferon alfa‐2b and ribavirin on steatosis in patients infected with hepatitis C (2003, background): “1a 250 (37) 117 (34) 133 (40) 68 (34) 182 (39) 150 (41) 112 (28) 38 (38) 1b 204 (31) 97 (28) 107 (33) 57 (29) 147 (31) 117 (32) 81 (25) 36 (36) 2 84 (13) 38 (11) 46 (14) 21 (11) 63 (13) 70 (19) 51 (19) 19 (19) 3 117 (17)* 82 (24) 35 (11)* 47 (24) 70 (15)* 17 (5) 11 (4) 6 (6) Other 15 (2) 7 (2) 8 (2)”
- Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes. (2014, background): “…overlapping pathophysiologies (Cope et al., 2000; Petrasek et al., 2013), and that steatosis (and occasionally steatohepatitis) is a hallmark of HCV genotype 3 infection (Rubbia-Brandt et al., 2000), it cannot be expected that the hepatic immune response we describe is exclusively found in NASH.”
- Genetic diversity and evolution of hepatitis C virus--15 years on. (2004, background): “…to the probable greater longterm pathogenicity of genotype 1, infections with genotype 3 are associated with a higher incidence of steatosis (Rubbia-Brandt et al., 2000; Adinolfi et al., 2001), which is thought to result from direct cytopathic damage to hepatocytes from a block in…”