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Expanding Cytotoxic T Lymphocytes from Umbilical Cord Blood that Target Cytomegalovirus, Epstein-Barr Virus, and Adenovirus
Published on: May 7, 2012
Hepatitis C virus - Associated marginal zone lymphoma
Marine Armand1, Caroline Besson2, Olivier Hermine3
1Department of Hematology, Hôpital Pitié-Salpêtrière, AP-HP, Paris, France; UPMC Univ Paris 06, UMRS-1138, Paris, France.
Insights
Hepatitis C virus (HCV) infection is linked to B-cell non-Hodgkin lymphoma, particularly marginal zone lymphoma (MZL) and diffuse large B-cell lymphoma (DLBCL). Antiviral treatment can lead to lymphoma regression, highlighting the virus's role in cancer development.
Area of Science:
- Virology
- Oncology
- Immunology
Background:
- The association between Hepatitis C Virus (HCV) infection and B-cell non-Hodgkin lymphoma (NHL) is well-established.
- Epidemiological studies and observed lymphoma regression post-HCV eradication support this link.
- Marginal Zone Lymphoma (MZL) and Diffuse Large B-cell Lymphoma (DLBCL) are the most frequently observed subtypes.
Purpose of the Study:
- To elucidate the role of HCV in lymphomagenesis.
- To explore proposed mechanisms linking HCV to lymphoma development.
- To assess the efficacy of antiviral therapy in treating HCV-associated lymphomas.
Main Methods:
- Review of epidemiological studies.
- Observation of lymphoma regression following antiviral treatment.
- Analysis of proposed pathogenetic mechanisms.
Main Results:
- HCV infection is a significant risk factor for developing MZL and DLBCL.
- Lymphoma regression is observed after successful HCV eradication.
- Proposed mechanisms include chronic B-cell receptor stimulation and direct viral protein effects.
Conclusions:
- Antiviral therapy, especially direct-acting antiviral agents, is effective and safe for treating HCV-associated MZL.
- Understanding HCV's role in lymphomagenesis is crucial for targeted treatment strategies.
- Further research into viral-host interactions can refine therapeutic approaches for HCV-related lymphomas.
Abstract:
The link between hepatitis C virus (HCV) infection and the development of B-cell non-Hodgkin lymphoma is now well established and based on a number of epidemiological studies. It is further supported by the observation of lymphoma regression after HCV eradication by antiviral treatment. The far most frequent entities are marginal zone lymphoma (MZL) and diffuse large B-cell lymphoma (DLBCL). MZL usually emerge on a background of mixed cryoglobulinemia, a low-grade lymphoproliferation, and often transform into DLBCL, thereby following a multistep oncogenesis process. The role of HCV in lymphomagenesis is not yet fully understood but several mechanisms have been proposed including (i) chronic external stimulation through the B-cell receptor and other surface receptors, and (ii) direct transformation by intracellular viral proteins, the former being probably predominant in MZL. Regression of HCV-associated MZL can be achieved with antiviral therapy and the novel generation of direct-acting antiviral agents appears highly effective and safe for the treatment of these lymphoma.
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