HBsAg-associated albumin receptors and antialbumin antibodies in sera of patients with liver disease.

Several investigators reported that sera from patients with liver disease react with polymerized human serum albumin. This reactivity may be mediated by antibodies to polymerized albumin or polymerized albumin receptor sites on HBsAg. We tested sera from 114 patients with a variety of liver diseases by techniques which differentiate polymerized albumin binding activity mediated by HBsAg-associated receptors from that due to immunoglobulins. Total polymerized albumin binding activity was detected by passive hemagglutination of polymerized albumin-coated red blood cells, in 62.3% of patients with liver disease. The specificity for polymerized albumin was proven by hemagglutination inhibition of 18 sera using polymeric, monomeric, and native albumin as inhibiting antigens. Indirect immunofluorescence of polymerized albumin coated red blood cells after incubation with serum revealed that antibodies, HBsAg or both mediated polymerized albumin binding. The predominant immunoglobulin class with polymerized albumin binding activity was IgG in sera from patients with chronic active hepatitis and alcoholic liver disease, and IgM in acute viral hepatitis, chronic persistent hepatitis, and primary biliary cirrhosis. HBsAg-mediated polymerized albumin binding activity was frequently associated with antibodies to polymerized albumin. The attachment of hepatitis B virus to hepatocytes may be facilitated by polymerized albumin via polymerized albumin receptors. Antibodies to polymerized albumin may interfere with this binding and may result in reduced infectivity.