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Antiviral Res. 2003 Oct;60(2):125-7.

Hepatitis C virus infection and liver steatosis.

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Liver Unit, Medical School of Lisbon, Av. GrĂ£o Vasco, 34-6 degrees D, 1500-338 Lisboa, Portugal.


The mechanism by which the hepatitis C virus (HCV) causes chronic, progressive liver damage is unknown. Factors other than the virus itself have been implicated. The role of liver steatosis has been recently studied. Hepatic steatosis is a common histological finding occurring in more 50% of patients with chronic hepatitis C. Both host and viral factors have been demonstrated to play an important role in its development. In those patients infected with genotype 1, steatosis appears to be due to the co-existence of Non-Alchoholic SteatoHepatitis (NASH) with HCV and associated with an increased body mass index (BMI). Some recent observations suggest that steatosis may be of viral origin and related to genotype 3. This fact raises the possibility of a direct effect of specific viral sequences on the pathogenesis of lipid accumulation. Furthermore, hepatic steatosis attributed to genotype 3 correlates directly with serum and intrahepatic titters of HCV RNA. The resolution of steatosis after successful antiviral therapy as well as steatosis being a sign of recurrent HCV infection in patients with genotype 3 add convincing evidence that steatosis is viral related. The pathogenic mechanism induced by genotype 3 is speculative. A correlation between steatosis, intrahepatic HCV RNA and core protein expression suggest a direct effect. Further support is provided by the finding that HCV core protein induces steatosis in transgenic mice. Another possibility relates to interaction with hepatic triglyceride turnover. In conclusion, for patients infected with genotype 1, BMI has a role in the pathogenesis of steatosis while in those infected with genotype 3, steatosis may be due to a virus-specific cytopathic effect. Regardless of etiology, the contribution of both to liver fibrosis progression seems accepted.

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