title: Pathogenesis and significance of hepatitis C virus steatosis: an update on survival strategy of a successful pathogen.
abstract: Hepatitis C virus (HCV) is a successful pathogen on the grounds that it exploits its host's metabolism to build up viral particles; moreover it favours its own survival by inducing chronic disease and the development of specific anatomic changes in the infected organ. Steatosis, therefore, is associated with HCV infection by necessity rather than by chance alone. Approximately 6% of HCV patients have steatohepatitis. Interestingly, HCV steatosis occurs in the setting of multiple metabolic abnormalities (hyperuricemia, reversible hypocholesterolemia, insulin resistance, arterial hypertension and expansion of visceral adipose tissue) collectively referred to as "hepatitis C-associated dysmetabolic syndrome" (HCADS). General, nonalcoholic fatty liver disease (NAFLD)-like, mechanisms of steatogenesis (including increased availability of lipogenic substrates and de novo lipogenesis; decreased oxidation of fatty substrates and export of fatty substrates) are shared by all HCV genotypes. However, genotype 3 seemingly amplifies such steatogenic molecular mechanisms reported to occur in NAFLD via more profound changes in microsomal triglyceride transfer protein; peroxisome proliferator-activated receptor alpha; sterol regulatory element-binding proteins and phosphatase and tensin homologue. HCV steatosis has a remarkable clinical impact in as much as it is an acknowledged risk factor for accelerated fibrogenesis; for impaired treatment response to interferon and ribavirin; and development of hepatocellular carcinoma. Recent data, moreover, suggest that HCV-steatosis contributes to premature atherogenesis via both direct and indirect mechanisms. In conclusion, HCV steatosis fulfills all expected requirements necessary to perpetuate the HCV life cycle. A better understanding of the physiology of HCADS will likely result in a more successful handling of disease with improved antiviral success rates.
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Amedeo
authors: A
authors: Lonardo
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Luigi Elio
authors: LE
authors: Adinolfi
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Luciano
authors: L
authors: Restivo
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Stefano
authors: S
authors: Ballestri
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Dante
authors: D
authors: Romagnoli
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Enrica
authors: E
authors: Baldelli
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Fabio
authors: F
authors: Nascimbeni
authors: Amedeo Lonardo, Stefano Ballestri, Dante Romagnoli, Enrica Baldelli, Fabio Nascimbeni, Paola Loria, Division of Internal Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41126 Modena, Italy.
authors: Paola
authors: P
authors: Loria
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000378:metabolism / Q000821:virology; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000821:virology; D005234:Fatty Liver / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism / Q000821:virology*; D016174:Hepacivirus / Q000187:drug effects / Q000254:growth & development / Q000472:pathogenicity*; D006526:Hepatitis C / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism / Q000821:virology*; D054884:Host-Pathogen Interactions; D006801:Humans; D050356:Lipid Metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000821:virology*; D008103:Liver Cirrhosis / Q000378:metabolism / Q000821:virology; D008113:Liver Neoplasms / Q000378:metabolism / Q000821:virology; D018384:Oxidative Stress; D011379:Prognosis; D012307:Risk Factors
chemical_list: D000998:Antiviral Agents
keywords: Atherosclerosis; Fibrosis; Hepatitis C virus; Hepatitis C-associated dysmetabolic syndrome; Hepatocellular carcinoma; Steatohepatitis; Sustained virological response