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Pathogenesis and significance of hepatitis C virus steatosis:An update on survival strategy of a successful pathogen

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World Journal of Gastroenterology 2014年第23期20卷 7089-7103页

作者： Amedeo Lonardo Luigi Elio Adinolfi Luciano Restivo Stefano Ballestri Dante Romagnoli Enrica Baldelli Fabio Nascimbeni paola loriaca Division of Internal Medicine Department of BiomedicalMetabolic and Neural SciencesUniversity of Modena and Reggio Emilia41126 ModenaItaly Department of Medical SurgicalNeurologicalMetabolicand Geriatric SciencesSecond University of Naples80100 NaplesItaly

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.

关键词： Atherosclerosis Fibrosis Hepatitis C-associated dysmetabolic syndrome Hepatocellular carcinoma Steatohepatitis Sustained virological response Hepatitis C virus

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