Fig. 1.
Fig. 1. An 18-month longitudinal study of the index case demonstrating the effect of IFN therapy on viral titers and the prevalence of IgMκ B cells. / Prelevalence of IgMκ (percentage of lymphocytes) with HCV viremia genomic equivalents (gEs) per milliliter during treatment with IFN (3 MU given daily [qd] or 3 times weekly [tiw] as previously described5) are demonstrated. Relapse was associated with marked lymphocytosis (lymphocyte count of 44 × 109/L [44 000/μL]), which was due predominantly to IgMκ B cells; a high level of viremia (7.3 × 107gE/mL), and a cryocrit of 4%. WBCs declined from 53.4 × 109/L to 5.0 × 109/L and lymphocytosis from 82% (lymphocyte count of 44 × 109/L) to 38% (lymphocyte count of 1.9 × 109/L) with IFN therapy. Decreases in IFN therapy from daily to 3 times weekly administration and interruption of therapy were accompanied by parallel increases in viremia and monoclonal B cells. Cryoglobulinemia fell to 1% cryocrit after 1 month of therapy and remained at trace levels (less than 1%) for the next 17 months. LDH returned to normal in May 1998 and remained within normal range throughout the remainder of the patient's course of treatment.

An 18-month longitudinal study of the index case demonstrating the effect of IFN therapy on viral titers and the prevalence of IgMκ B cells.

Prelevalence of IgMκ (percentage of lymphocytes) with HCV viremia genomic equivalents (gEs) per milliliter during treatment with IFN (3 MU given daily [qd] or 3 times weekly [tiw] as previously described5) are demonstrated. Relapse was associated with marked lymphocytosis (lymphocyte count of 44 × 109/L [44 000/μL]), which was due predominantly to IgMκ B cells; a high level of viremia (7.3 × 107gE/mL), and a cryocrit of 4%. WBCs declined from 53.4 × 109/L to 5.0 × 109/L and lymphocytosis from 82% (lymphocyte count of 44 × 109/L) to 38% (lymphocyte count of 1.9 × 109/L) with IFN therapy. Decreases in IFN therapy from daily to 3 times weekly administration and interruption of therapy were accompanied by parallel increases in viremia and monoclonal B cells. Cryoglobulinemia fell to 1% cryocrit after 1 month of therapy and remained at trace levels (less than 1%) for the next 17 months. LDH returned to normal in May 1998 and remained within normal range throughout the remainder of the patient's course of treatment.

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