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A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Hepatitis C
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8887.
Insights
Hepatitis C virus (HCV) causes chronic post-transfusion hepatitis. Detecting anti-HCV antibodies aids diagnosis, and blood screening may prevent future infections.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Hepatitis C virus (HCV) identified as the primary cause of chronic post-transfusion hepatitis.
- HCV is a single-stranded RNA virus, similar to flaviviruses.
- Hepatitis E virus (HEV) linked to epidemic, enterically-transmitted non-A, non-B hepatitis.
Purpose of the Study:
- To summarize current understanding of Hepatitis C virus (HCV) in post-transfusion hepatitis.
- To review diagnostic markers and therapeutic approaches for HCV infection.
- To discuss the potential of blood screening for HCV prevention.
Main Methods:
- Review of existing literature on Hepatitis C virus (HCV) and non-A, non-B hepatitis.
- Analysis of anti-HCV antibody detection in patients and blood donors.
- Evaluation of interferon therapy outcomes for chronic hepatitis C.
Main Results:
- Anti-HCV antibodies are present in up to 90% of chronic non-A, non-B post-transfusion hepatitis patients.
- HCV antibodies found in 1% of blood donors and implicated donors, plus patients with autoimmune liver disease and hepatocellular carcinoma.
- Recombinant human alpha-interferon therapy improves aminotransferase levels in ~50% of patients, but relapse is common.
Conclusions:
- HCV is the main cause of chronic post-transfusion hepatitis, detected via anti-HCV antibodies.
- HCV infection may impact alcoholic liver disease; its role in fulminant hepatitis and aplastic anemia requires further study.
- Future blood screening for HCV could significantly reduce post-transfusion hepatitis cases.
Abstract:
The major cause of chronic post-transfusion hepatitis, the hepatitis C virus (HCV), has been identified. HCV is a single-stranded linear RNA virus with characteristics similar to the flaviviruses. A different agent, the hepatitis E virus, is associated with epidemic (enterically-transmitted) non-A, non-B hepatitis. At present, infection with HCV is recognized by the finding of anti-HCV antibodies, positive in up to 90% of patients with chronic non-A, non-B post-transfusion hepatitis. Antibodies to HCV are detected in 1% of normal volunteer blood donors and in the majority of donors implicated in post-transfusion hepatitis. HCV antibodies are also found in patients with autoimmune liver disease and hepatocellular carcinoma. Moreover, HCV infection may contribute to the pathogenesis of liver disease in alcoholic patients. The role of HCV infection in fulminant non-A, non-B hepatitis and hepatitis-associated aplastic anemia has not been elucidated as yet. Therapy of chronic non-A, non-B hepatitis with recombinant human alpha-interferon has been shown to improve or normalize aminotransferase levels in approximately 50% of patients, most of whom have evidence of HCV infection. However, relapse after cessation of treatment is common. In the future, screening blood for evidence of HCV infection may prevent most cases of non-A, non-B post-transfusion hepatitis.
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