Hepatitis C-associated B-cell non-Hodgkin lymphomas. Epidemiology, molecular signature and clinical management

Jan Peveling-Oberhag, Luca Arcaini, Martin Leo Hansmann, Stefan Zeuzem

Research output: Contribution to journalArticlepeer-review

Abstract

There is ample epidemiologic evidence for an association of chronic hepatitis C virus (HCV) infection with B-cell non-Hodgkin lymphoma (B-NHL). B-NHL subtypes most frequently associated with HCV are marginal zone lymphoma and diffuse large B-cell lymphoma. The most convincing evidence for a causal relationship between HCV infection and lymphoma development is the observation of B-NHL regression after HCV eradication by antiviral therapy (AVT). In fact, for indolent HCV-associated B-NHL, first-line AVT instead of standard immune-chemotherapy might be considered. Molecular mechanisms of HCV-NHL development are still poorly understood. Three general theories have emerged to understand the HCV-induced lymphomagenesis: (1) continuous external stimulation of lymphocyte receptors by viral antigens and consecutive proliferation; (2) HCV replication in B cells with oncogenic effect mediated by intracellular viral proteins; (3) permanent B-cell damage, e.g., mutation of tumor suppressor genes, caused by a transiently intracellular virus ("hit and run" theory). This review systematically summarizes the data on epidemiology, interventional studies, and molecular mechanisms of HCV-associated B-NHL.

Original languageEnglish
Pages (from-to)169-177
Number of pages9
JournalJournal of Hepatology
Volume59
Issue number1
DOIs
Publication statusPublished - Jul 2013

Keywords

  • Antiviral therapy
  • B-cell
  • Hepatitis C
  • Lymphoma
  • Non-Hodgkin lymphoma

ASJC Scopus subject areas

  • Hepatology

Fingerprint Dive into the research topics of 'Hepatitis C-associated B-cell non-Hodgkin lymphomas. Epidemiology, molecular signature and clinical management'. Together they form a unique fingerprint.

Cite this