Hepatitis C virus (HCV) infection induces the ␣-chemokine interleukin-8 (CXCL-8Hepatitis C virus (HCV) infects an estimated 3% or 170 million of the world's population and causes an estimated 476,000 deaths per year due to complications of end-stage liver disease (56,62). In the United States, about 1.8% of the general population or 4 million persons are infected. Of those acutely infected with HCV, approximately 85% develop chronic infection, and about 70% of these patients develop histological evidence of chronic liver disease. Moreover, viremia is not cleared in about 50% of infected patients treated with pegylated interferon (IFN)-ribavirin therapy, the current standard of care. Compounding this issue are the predictions that in the next 20 years, HCV-related complications, including hepatic decompensation, hepatocellular carcinoma, and liverrelated deaths, will increase by 106%, 81%, and 180%, respectively (12). Thus, chronic hepatitis C is a serious global medical problem necessitating effective treatment. Given the propensity of HCV for chronic infection, association with severe liver disease, and difficulty of treatment, many studies are focused on HCV-host interactions that contribute to HCV persistence and pathogenesis.

The data suggest that increased CXCL-8 gene expression in the context of HCV replication involves posttranscriptional events.