Chronic hepatitis C infection has been associated with increased collagen deposition leading to hepatic fibrosis and cirrhosis. The mechanism of hepatocarcinogenesis is unclear. The role of oxidative stress secondary to chronic inflammation has been implicated which may produce oxidative DNA damage. It is critically important to understand the evolution of the disease in young subjects, because these subjects have the longest potential benefit from antiviral therapy and strategies to prevent the development of liver fibrosis, cirrhosis and cancer. In addition, children are biologically naive, so an in depth study of HCV in children (who are free of alcoholism and other confounding variables) could yield a clearer understanding of the hepatogenesis of the virus.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
3M01RR000052-38S1
Application #
6297537
Study Section
Project Start
1998-12-01
Project End
1999-11-30
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
38
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Johns Hopkins University
Department
Type
DUNS #
045911138
City
Baltimore
State
MD
Country
United States
Zip Code
21218
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