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The pathogenesis of the anemia in 17 horses experimentally infected with the virus of equine infectious anemia (EIA) was investigated. It was demonstrated by direct Coombs' tests that 15 of the animals had C′3 but no IgG, IgM or IgG(T) on their RBC surfaces. Red blood cells from 8 of 10 horses with a positive anti-C′3 Coombs' test were more osmotically fragile than normal. The RBC life spans of 7 horses with C′3 coated RBC ranged from 18 to 90 days (normal 136 ± 17 days). It was concluded that the hemolysis in this virus disease was associated with C′3 coating of RBC.

The role of non-complement-fixing anti-equine infectious anemia (EIA) antibody in the conversion of complement fixation (CF) tests from positive to negative in EIA-infected horses was investigated. Complement-fixation inhibition (CFI) tests demonstrated antibodies in sera that were CF negative. These antibodies would bind to antigen, but would not fix complement. The inhibiting antibodies were isolated and shown to be IgG(T) by immunoelectrophoresis and immunodiffusion against monospecific anti-IgG(T) antisera. Separation of immunoglobulins from affected horse sera by DEAE cellulose chromatography revealed 11 of 13 had complement-fixing IgG and non-complement-fixing IgG(T) antibodies present simultaneously regardless of the reactivity of whole sera. The reactivity of whole sera in CF and CFI tests evidently depended upon the relative concentration and perhaps affinity of the Ig classes. The predominant class fluctuated in serial sera from four of six persistently infected horses.

There is increasing evidence that complement-dependent immune reactions are pathogenetically important in virus diseases. One indication of in vivo complementfixing immune reactions is the lowering of plasma C3 levels. A study was made of the circulating plasma C3 levels in 12 horses infected with equine infectious anemia (EIA) virus. Purified equine C3 was prepared from euglobulin precipitates of horse serum using triethylaminoethyl (TEAE) column chromatography with subsequent Pevikon block electrophoresis. Monospecific antisera prepared in rabbits was used in single radial immunodiffusion to quantitate C3 levels. A significant reduction of C3 was detected in 6 of 12 horses with active clinical disease. All horses with reduced C3 levels had C3-coated erythrocytes and deposits of immunoglobulin and C3 in the glomeruli. These findings further indicate that immune processes are active in the pathogenesis of EIA.

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).