Feb 25, 2012
It has been shown that HCV genotype 3 is independently associated with hepatocellular steatosis in patients with chronic hepatitis C.  Furthermore, the severity of steatosis in these patients is directly related to the burden of the HCV RNA load. This relationship between the HCV viral load and the magnitude of steatosis was not observed in other HCV genotypes.  It has also been noticed that the steatosis which was initially present in patients with genotype 3 infection resolves after a sustained virologic response is achieved through treatment with pegylated interferon-α and ribavirin.  Not only does the steatosis resolve with eradication of the virus but it also recurs if relapse transpires. All of these findings were only observed with the HCV genotype 3 virus and was not reproducible with other HCV genotypes. These findings all point to the ability of the HCV genotype 3 virus to directly induce steatosis, although the mechanism still remains elusive.
Thus, there seems to be two distinct forms of steatosis in patients with chronic hepatitis C. Metabolic steatosis generally occurs in all genotypes of HCV infections and likely worsens the progression of HCV induced fibrosis. Then there are those patients with genotype 3 infections who have a form of steatosis that is directly induced by the hepatitis C virus and which also resolves with successful treatment. These two forms of steatosis can certainly coexist in patients with genotype 3 infections with other underlying metabolic diseases. In these patients, we would expect that the steatosis would only partially resolve with successful eradication of the virus and that the remaining fatty infiltration is a result of NAFLD.