Hepatitis C virus infection: Racial differences in presentation, progression and response to therapy

This dissertation examines differences in the epidemiology of hepatitis C virus (HCV) infection between African Americans and Caucasians diagnosed at the Atlanta Veterans Affairs Medical Center (AVAMC). Medical and laboratory records of 2,152 AA and 1,118 Caucasian patients diagnosed between 1992 and 2003 were reviewed in a retrospective study to compare the virological, biochemical and clinical features at diagnosis and the progression of liver disease in the two races. Survival experience of infected (165 African American, 79 Caucasian) and non-infected (307 African American, 197 Caucasian) patients who had serological tests for HCV between 1992 and 1995 was compared controlling for major co-morbid conditions. Racial difference in the response to anti-HCV therapy was assessed in 71 AA and 87 Caucasians receiving ribavirin and either pegylated interferon or interferon alpha. African Americans had more persistent infection as evidenced by their higher rate of detectable HCV viremia among all patients with anti-HCV antibody and tended to have a poorer response to anti-HCV therapy. In contrast, African Americans had less hepatic necroinflammatory activity as evidenced by lower serum levels of ALT, AST & bilirubin; lower prevalence of advanced stages of liver disease despite similar age distributions, and a slower rate of progression to cirrhosis despite higher prevalence of negative factors including alcohol and drug abuse. HCV infection was not an independent predictor of poor survival in multivariate analysis. Race was a significant modifier of the effect of HCV infection on the survival of patients. The deleterious effect of HCV infection on survival was more severe in Caucasians than in African Americans. These findings may be caused by differences in HCV specific immune response in the two races. It is possible that African Americans develop certain immunologic tolerance to HCV that allows the persistence of the infection with a lesser or slower injury to the host. Further laboratory-based research is warranted to identify the biologic basis behind these epidemiologic observations.