A number of proposals have been suggested to explain the mechanism of plasmacytosis and hypergammaglobulinemia in mink infected with Aleutian disease (AD) virus. That the virus induces a myeloma-like proliferation of plasma cells and the production of immunoglobulins not directed toward specific antigens was suggested by several workers (1–5). The transition from polyclonal to monoclonal gammopathies in 10% to 20% of the infected mink with genotypes Aa and AA (non-Aleutian mink) supports this suggestion (2). However, detection of anti-virus antibody in the form of infectious virus-antibody complexes (6) and by direct and indirect immunofluorescence on infected tissue (7; J. B. Henson and T. B. Crawford, manuscript in preparation) demonstrates that some of the hypergammaglobulinemia represents antibody to AD viral antigens. A previous attempt by other investigators to demonstrate complement-fixation (CF) between AD-affected sera and infectious organ homogenates was unsuccessful (1).