Receptors for polymerized human albumin are found at high titres during high-level hepatitis B virus (HBV) replication and in small amounts in chronic low-level infection. Complexes between hepatitis B surface antigen (HBsAg) and IgM without specificity for HbsAg are expressed in a pattern similar to that of receptors. Anti-albumin antibodies could be involved in their formation. Delta infection depresses the synthesis of gene products of HBV. To assess whether delta modifies the expression of receptors on HBsAg and the level of HBsAg/IgM complexes, and if anti-albumin antibodies are actually part of the complex, we tested sera from 86 subjects with acute and chronic HBV infection. Our findings show that the amounts of circulating receptors and HBsAg/IgM are proportional to the concentration of HBsAg and thus probably to the degree of viral replication. We did not find any correlation between circulating anti-albumin antibodies of the IgM class and HBsAg/IgM complexes. Delta infection depresses HBsAg synthesis and causes a related decrease in receptors and HBsAg/IgM titres if superimposed on the more active stage of HBV infection. When HBsAg, receptors, and HBsAg/IgM are at low levels, no further depression is caused by delta infection. HBsAg/IgM titre is not enhanced by presence of anti-delta antibodies, thus excluding a role of the latter in forming these complexes.