Abstract

Approximately 0.6% of the volunteer donor population has been found to have antibody to the hepatitis C virus (anti-HCV), the predominant cause of transfusion associated hepatitis (TAH). Some of the donors are true positive as determined by a recombinant immunoblot assay (RIBA) and some are false positives and some are RIBA indeterminate. This study will enroll at least 100 anti-HCV positive donors in each of the RIBA categories and compare epidemiologic risk factors for HCV acquisition and the extent of associated liver disease. Preliminary analysis reveals that at least 70% of RIBA positive donors have recognized parenteral risk factors, primarily IV drug use compared to less than 5% of controls. These risk factors should have excluded these individuals from donation, but failed to do so indicating the need for revision of donor screening procedures. Approximately 80% of asymptomatic RIBA positive donors have biochemical evidence of chronic hepatitis and 80% also have detectable HCV RNA.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
Clinical Center (CLC)
Type
Intramural Research (Z01)
Project #
1Z01CL002068-03
Application #
3752237
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
3
Fiscal Year
1994
Total Cost
Indirect Cost

  Institution

Name
Clinical Center
Department
Type
DUNS #
City
State
Country
United States
Zip Code

  Publications

Alter, Harvey J (2013) The road not taken or how I learned to love the liver: A personal perspective on hepatitis history. Hepatology :
Makuria, Addisalem T; Raghuraman, Sukanya; Burbelo, Peter D et al. (2012) The clinical relevance of persistent recombinant immunoblot assay-indeterminate reactions: insights into the natural history of hepatitis C virus infection and implications for donor counseling. Transfusion :
Hanada, Kousuke; Tanaka, Yasuhito; Mizokami, Masashi et al. (2007) A reduction in selective immune pressure during the course of chronic hepatitis C correlates with diminished biochemical evidence of hepatic inflammation. Virology 361:27-33
Huang, Ying; Yang, Huiying; Borg, Brian B et al. (2007) A functional SNP of interferon-gamma gene is important for interferon-alpha-induced and spontaneous recovery from hepatitis C virus infection. Proc Natl Acad Sci U S A 104:985-90
Tanaka, Yasuhito; Kurbanov, Fuat; Mano, Shuhei et al. (2006) Molecular tracing of the global hepatitis C virus epidemic predicts regional patterns of hepatocellular carcinoma mortality. Gastroenterology 130:703-14
Umemura, Takeji; Wang, Richard Y-H; Schechterly, Cathy et al. (2006) Quantitative analysis of anti-hepatitis C virus antibody-secreting B cells in patients with chronic hepatitis C. Hepatology 43:91-9
Farci, Patrizia; Quinti, Isabella; Farci, Stefania et al. (2006) Evolution of hepatitis C viral quasispecies and hepatic injury in perinatally infected children followed prospectively. Proc Natl Acad Sci U S A 103:8475-80
Sugimoto, Kazushi; Kaplan, David E; Ikeda, Fusao et al. (2005) Strain-specific T-cell suppression and protective immunity in patients with chronic hepatitis C virus infection. J Virol 79:6976-83
Rahman, Fareed; Heller, Theo; Sobao, Yuji et al. (2004) Effects of antiviral therapy on the cellular immune response in acute hepatitis C. Hepatology 40:87-97
Ghany, Marc G; Kleiner, David E; Alter, Harvey et al. (2003) Progression of fibrosis in chronic hepatitis C. Gastroenterology 124:97-104

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