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T(14;18) translocation in chronic hepatitis C virus infection

A L Zignego1, F Giannelli, M E Marrocchi

  • 1Department of Internal Medicine, University of Florence, School of Medicine, 50134 Florence, Italy. a.zignego@dfc.unifi.it

Hepatology (Baltimore, Md.)
|February 3, 2000
PubMed

Insights

The t(14;18) translocation and bcl-2 over-expression are common in chronic hepatitis C virus (HCV) infection, potentially contributing to B-cell lymphoproliferative disorders. This finding sheds light on HCV pathogenesis.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Pathogenic mechanisms of B-cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection remain unclear.
  • HCV infection is associated with various B-cell abnormalities and lymphoproliferative disorders.

Purpose of the Study:

  • To investigate the frequency of t(14;18) translocation and bcl-2 over-expression in patients with chronic HCV infection.
  • To explore the potential role of t(14;18) translocation in the pathogenesis of HCV-related lymphoproliferative disorders.

Main Methods:

  • Polymerase chain reaction (PCR) was used to detect t(14;18) translocation in peripheral blood mononuclear cells.
  • Immunoblot analysis was performed to assess bcl-2 over-expression.
  • Patient groups included those with HCV-related liver disease, mixed cryoglobulinemia syndrome, HCV-negative liver disease, and controls.

Main Results:

  • T(14;18) translocation was significantly more frequent in patients with HCV-related liver disease (26%) and mixed cryoglobulinemia syndrome (71.4%) compared to controls (3.6%-3.3%).
  • All t(14;18)-positive samples exhibited bcl-2 over-expression.
  • A higher prevalence of serum cryoglobulins was observed in HCV patients with t(14;18) translocation.

Conclusions:

  • T(14;18) translocation and bcl-2 over-expression are frequent in chronic HCV infection.
  • These genetic alterations may contribute to the development of HCV-related lymphoproliferative disorders.
  • The findings provide insights into the molecular pathogenesis of HCV-associated B-cell malignancies.

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