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

J Hepatol. 2013 Jul;59(1):169-77. doi: 10.1016/j.jhep.2013.03.018. Epub 2013 Mar 27.

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.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Antiviral Agents / therapeutic use
  • B-Lymphocytes / immunology
  • B-Lymphocytes / virology
  • Hepacivirus / immunology
  • Hepacivirus / pathogenicity
  • Hepatitis C Antigens
  • Hepatitis C, Chronic / complications*
  • Hepatitis C, Chronic / drug therapy
  • Hepatitis C, Chronic / epidemiology
  • Humans
  • Lymphoma, B-Cell / drug therapy
  • Lymphoma, B-Cell / epidemiology
  • Lymphoma, B-Cell / etiology*
  • Models, Biological
  • Risk Factors

Substances

  • Antineoplastic Agents
  • Antiviral Agents
  • Hepatitis C Antigens