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ABSTRACT— Forty‐seven patients with chronic hepatitis C were treated with recombinant interferon alpha‐2a (rIFNα2a) given subcutaneously in a standard dose of 3 MU thrice weekly for 12 months. Stored baseline sera and monthly samples during treatment were assayed for anti‐interferon neutralizing antibodies using the antiviral neutralization bioassay against 5 IU of rIFNα2a. During therapy, 15 of 47 patients (31.9%) developed detectable levels of neutralizing antibodies within 2–8 months after starting treatment. After 12 months of therapy, 26 of 32 antibody‐negative patients (81.3%) showed normalization or marked reduction of ALT levels compared to 4 of 15 (26.6%) who developed anti‐IFN neutralizing antibodies (p = 0.0009). Four patients demonstrated antiviral response during treatment even in the presence of low levels or late occurrence of neutralizing antibodies. Six of the seven patients who had disease reactivation after an initial response developed high titers of neutralizing antibodies. Our results suggest that reactivation of chronic hepatitis C before completion of therapy seems to be an obvious consequence of anti‐IFN neutralizing antibody formation.

We studied the incidence of specific antibodies to interferon-a2 (IFN-a2) in 251 patients with chronic hepatitis C treated with recombinant IFN-a2a, and the time when these antibodies developed. Neutralizing antibodies (N.Ab) were found in 23.1% of the patients, and binding antibodies (B.Ab) in Address reprint requests to:

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A study was performed on a family of 7 followed up over a 4-year period in which an outbreak of B-antigen-positive hepatitis occurred. Of the 5 male members who acquired HB_sAg, 1 became a chronic asymptomatic carrier and 4 had episodes of acute icteric hepatitis during a 15-month period with development of histologically documented chronic hepatitis with persistent HB_S antigenaemia in all. Of the 2 female members, 1 had an attack of acute HB_sAg-positive hepatitis but recovered normally and cleared HB_sAg from her serum, while the other was found to have anti-HB_s with no evidence of liver disease. Serological and immunological studies carried out in all members of this family suggested that a sex-linked defect of T cell function itself could explain the differing host immune response to HBV infection in genetically related subjects.

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