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Non–organ-specific autoantibodies, including antinuclear antibodies, anti–smooth muscle antibodies, and anti–liver/kidney microsomal type 1 antibodies, are present in about one third of patients with chronic hepatitis C. Two theories of autoantibody generation in patients with hepatitis C are proposed. The first proposes that the binding of hepatitis C virus to CD81 on B-lymphocytes lowers the activation threshold of these cells, thus facilitating the production of autoantibodies. The second proposes that the autoantibodies are produced through molecular mimicry. Unfortunately, the pathogenic role of these autoantibodies remains controversial. In addition, whether the autoantibodies can adversely affect treatment outcomes when patients receive interferon-α is unclear. Although the presence of autoantibodies in patients with hepatitis C is not considered a contraindication to interferon therapy, patients should be monitored carefully while on therapy.

End-stage liver disease associated with hepatitis C virus (HCV) infection is the most common indication for liver transplantation in the United States. Recurrent HCV infection is nearly universal and disease progression is accelerated in the immunocompromised host. In the post-transplant setting, the HCV-specific immune response plays a critical role in viral surveillance and disease progression. A failure to mount an efficient response to HCV antigens, either because of selective defects in the host immune system or because of viral interference with the normal function of the immune cells, could account for the inability of most transplant recipients to eradicate HCV.