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A transgenic mouse model of steatosis and hepatocellular carcinoma associated with chronic hepatitis C virus infection in humans.

Chronic hepatitis C is a necroinflammatory disease of the liver that is caused by infection with hepatitis C virus (HCV) (1). Uniquely adapted to establish persistent infections within the human liver, the major pathologic hallmark of this flavivirus infection is the insidious progression of hepatic fibrosis and loss of functioning hepatocyte mass (2-4). Typically, this occurs against a background of chronic hepatic inflammation and associated macroand microvesicular steatosis. A significant proportion of infected persons ultimately develop cirrhosis, hepatic failure, or hepatocellular carcinoma (HCC) (5-7). These lethal manifestations of hepatitis C are currently thought to result in approximately 8,000-10,000 deaths annually among the 3.9 million Americans infected with this virus (8). This makes hepatitis C the single most common cause of clinically significant liver disease in the United States today. Despite this, little is known about the molecular mechanisms underlying the chronic hepatic changes that are associated with this viral infection. However, it is generally believed that most if not all of the pathologic consequences of hepatitis C arise as a result of the cellular immune response to the infection, and that the infection itself is likely to be noncytopathic. Existing therapies for chronic hepatitis C include recombinant human interferon, either alone or in combination with ribavirin (9,10). These antiviral therapies are only partially effective, leading to the