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Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
No association between hepatitis C and B-cell lymphoma
J D Collier1, B Zanke, M Moore
1Department of Medicine, Princess Margaret Hospital, Toronto, Canada.
Insights
Hepatitis C virus (HCV) and GBV-C are unlikely to cause B-cell lymphoma in North America. Testing found no significant link between these viruses and lymphoma in patients from a low-prevalence region.
Area of Science:
- Virology
- Oncology
- Immunology
Background:
- Chronic viral infections, including hepatitis C virus (HCV), are suspected in B-cell lymphoma development.
- HCV infects lymphocytes and may trigger B-cell proliferation.
- Co-infection with GB virus type C (GBV-C) is common in HCV-infected individuals.
Purpose of the Study:
- To determine the prevalence of HCV and GBV-C infections in North American patients with B-cell lymphoma.
- To investigate the potential role of these viruses in B-cell lymphoma pathogenesis in a low-prevalence area.
Main Methods:
- Serum samples from 100 B-cell lymphoma patients and 100 controls with nonhematological malignancies were analyzed.
- HCV antibodies were detected using third-generation ELISA.
- HCV RNA and GBV-C RNA were quantified using reverse transcriptase PCR.
Main Results:
- No antibodies to HCV were detected in either lymphoma patients or controls.
- HCV RNA was not found in 60% of lymphoma patients.
- GBV-C RNA was detected in 5% of lymphoma patients and 3% of controls.
Conclusions:
- Hepatitis C virus and GBV-C are unlikely to be major contributors to B-cell lymphoma pathogenesis in North America.
- The study suggests a limited role for these specific viral infections in the development of B-cell lymphomas in this population.
- Further research may explore other potential viral or environmental factors in lymphoma development.
Abstract:
Chronic viral infection has been implicated in the pathogenesis of B-cell lymphoma, and hepatitis C virus (HCV) infects lymphocytes. Chronic infection with HCV may result in B-cell proliferation. Individuals infected with hepatitis C are often co-infected with the RNA virus GB virus type C. Studies from Europe where hepatitis C infection is more common than in North America have shown a high prevalence of hepatitis C infection in patients with B-cell lymphoma. The aim of this study was to establish the prevalence of HCV and GBV-C infection in patients with B-cell lymphoma in an area of low HCV prevalence. One hundred patients with B-cell lymphoma (10 high grade, 46 intermediate grade, and 44 low grade) and 100 controls with nonhematological malignancies were studied. Serum was analyzed for HCV antibodies by third generation enzyme-linked immunosorbant assay, and HCV RNA and GBV-C RNA was analyzed by reverse transcriptase PCR. None of the controls or lymphoma patients had antibodies to HCV. HCV RNA was undetected in 60 out of 100 lymphoma patients tested. GBV-C RNA was detected in the serum of 5 out of 100 (5%) of lymphoma patients and in 3 out of 100 (3%) controls. Hepatitis C and GBV-C are, therefore, unlikely to play a major role in the pathogenesis of B-cell lymphoma in North America.
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