Interferon-a elicits antiviral and immunoregulatory activities by binding to specific receptors on the cell surface. In this study, binding characteristics of interferon-a to peripheral blood mononuclear cells in patients with chronic hepatitis B virus infection were studied using radioiodinated recombinant interferon-QZ,, to determine interferon-a receptor numbers and dissociation constants. A single class of interferon-a receptor was demonstrated on peripheral blood mononuclear cells and mononuclear subsets. Peripheral blood mononuclear cells from patients with chronic hepatitis B virus infection (n = 20) and controls (n = 16) expressed a similar number of interferon-a receptors (484 ? 175 vs. 511 168 sites/cell respectively, p = NS) with a similar dissociation constant (dissociation constant = 0.2 to 0.7 nmol/L). Expression of interferon-a receptors was similar in monocyteenriched and lymphocyte-enriched fractions in both groups. Similar changes were observed in patients receiving a-interferon therapy. There was no correlation between interferon-a receptors expression and serum transaminase, serum HBsAg, serum HBV DNA, liver histological findings or the response to interferon-a therapy.
After incubation of lymphocytes in uitro with interferon-a,, (10 to 1,000 U/ml), interferon-a receptors number dropped by 42% to 80%, but this was associated with an increase in binding affinity (dissociation constant -0.05 to 0.15 nmoln) in both patients and controls. There was significant delay in the initial phase of receptor recovery in the patients with chronic hepatitis B virus infection compared with normal controls (days 1 and 2, p < 0.05).
These data indicate that interferon-a receptors are expressed and regulated normally in chronic hepatitis B virus infection and that the variable response to interferon-a therapy is not due to a variation in interferon-a receptor. The increase in binding affinity on interferon-a therapy may be one factor explaining