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Blood, 15 March 2001, Vol. 97, No. 6, pp. 1555-1559
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
The effect of antiviral therapy on t(14;18) translocation and
immunoglobulin gene rearrangement in patients with chronic hepatitis C
virus infection
Eli Zuckerman,
Tsila Zuckerman,
Dvora Sahar,
Sara Streichman,
Dina Attias,
Edmond Sabo,
Daniel Yeshurun, and
Jacob M. Rowe
From the Liver Unit and the Department of Internal
Medicine A, and the Institute of Hematology, Bnai Zion Medical Center;
Division of Hematology, Rambam Medical Center, and Department of
Pathology, Carmel Medical Center, Bruce Rappaport Faculty of Medicine,
Technion, Israel Institute of Technology, Haifa, Israel.
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. Thus,
this study investigated the effect of antiviral treatment on
immunoglobulin heavy-chain gene (IgH) rearrangement and t(14;18)
translocation in HCV infected patients. Twenty-nine patients with
chronic HCV infection were studied in whom IgH rearrangement and/or
t(14;18) translocation were previously detected. The IgH rearrangement (FR3/JH) and t(14;18) translocation (MBR
bcl2-JH) were detected in peripheral blood mononuclear
cells by polymerase chain reaction. Fifteen of 29 patients (8 with IgH
rearrangement, 6 with t(14;18) translocation, and 1 with both) were
treated with either interferon- or by combination therapy with
interferon and ribavirin for 6 to 12 months. IgH rearrangement became
negative in 7 of 9 treated patients compared with only 1 of 8 of
nontreated patients (P < .02). The t(14;18)
translocation became negative in 6 of 7 treated patients compared with
1 of 6 nontreated patients (P = .03). Disappearance of
IgH rearrangement or t(14;18) translocation was strongly associated with virologic response to treatment. Two t(14;18)+
patients developed B-cell lymphoma during follow-up. Antiviral treatment appears to be effective in eliminating the clonal
proliferation of B cells in patients with chronic HCV infection and may
prevent the subsequent development of lymphoma. The mechanism can be
related to a direct effect of interferon- on the proliferating clone or to an indirect effect by eradicating the antigenic stimulus.
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