B-cell clonality and t(14;18) in Egyptian patients with chronic hepatitis C and its relation to antiviral therapy

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The mechanism of lymphomagenesis of hepatitis C virus (HCV)-related B-cell lymphoma is unknown. Recently, it has been suggested that HCV may induce B-cell clonal proliferation and t(14;18) translocation in patients chronically infected with the virus.


The aim of this study was to assess the occurrence of immunoglobulin heavy chain (IgH) gene rearrangement and t(14;18) translocation in Egyptian chronic HCV patients and to examine the effect of antiviral treatment on IgH rearrangement and t(14;18) in HCV-infected patients.

Patients and methods

Forty-five Egyptian patients with chronic HCV infection were selected. The level of HCV-RNA in the serum was quantified using the Stratagene Mx3000P Real-Time PCR System at diagnosis and 3, 6, and 12 months from the beginning of the therapy. IgH clonality was detected using multiplex VH-JH (FR2) PCR, whereas t(14;18) was detected using nested PCR before and after antiviral therapy.


After 3 months of antiviral therapy, 24/45 patients (53.3%) showed an early virological response and completed their 12 months of antiviral therapy, after which they showed complete clearance of serum HCV-RNA (responder group). However, 21/45 patients (46.7%) did not show early virological response and hence stopped their therapy (nonresponder group). Clonal IgH rearrangement and t(14;18) were detected in 33.3 and 40% of patients, respectively. The percentage of patients who lose their clonal IgH or t(14;18) varies according to the completion of antiviral therapy. On comparing responder (12 months therapy) versus nonresponder (3 months therapy) groups, the loss of clonal IgH was nonsignificant (100 vs. 66.7%, P=0.134) whereas it was highly significant in terms of regression in t(14;18) (75 vs. 0%, P=0.0006).


In Egyptian patients with chronic HCV infection, the presence of clonal B cell and t(14;18) is a frequent finding. Twelve months of antiviral therapy are efficiently effective for regression of clonal IgH gene rearrangement and t(14;18).

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