439 I148m Pnpla3 Variant Promotes Steatosis According to Viral and Il28b Genotype but Does Not Affect Sustained Viral Response in Patients With Hepatitis C

A Variant in PNPLA3 Associated With Fibrosis Progression but not Hepatocellular Carcinoma in Patients With Hepatitis C Virus Infection

“…The biological role of PNPLA3 is debated but it likely facilitates fat accumulation in hepatocytes, potentially via interfering with lipoprotein export and favoring lipogenic activity over lipase activity [19,20]. PNPLA3 does not appear to have a direct effect on HCV infection, with prior studies showing no association with viral load or treatment response [21]. These data have lead some investigators to question the potential association between PNPLA3 and degree of fibrosis in patients with HCV and other non-steatosis liver diseases.…”

Genome-Wide Association Studies and Hepatitis C: Harvesting the Benefits of the Genomic Revolution

“…Several studies reported an association between the IFNL responder genotype and less frequent hepatic steatosis in HCV-1, [99][100][101] while other studies failed to find any significant association. 102,103 In the setting of liver transplantation for CHC, a recent reported suggested that donor rs12979860 TT had an increased incidence of graft steatosis over time, independent of HCV genotype, while recipient genotype was not associated with steatosis. 104 Two recent studies show evidence of an interaction between IFNL rs12979860 and the PNPLA3 rs738409 polymorphism and hepatic steatosis.…”