1. Rh0(D) positive red cells treated with periodate or mumps virus were not agglutinated by anti-Rh sera containing specific saline agglutinins. Agglutinability was restored by trypsinization.
2. Eluates from periodate or mumps-treated Rh0(D) erythrocytes or stromata inhibited agglutination of both normal and trypsinized Rh0(D) cells by specific antiserum. Eluates from Rh0(D) negative cells or stromata were not inhibitory. No inhibition was demonstrable with eluates from Rh0(D) cells treated with influenza or Newcastle disease viruses.
3. Eluates from periodate or mumps-treated Rh0(D) cells or stromata formed precipitates when mixed with anti-Rh0(D) serum. The virus-treated cell eluates were more effective in producing precipitation.
4. Titers of anti-Rh inhibitor in eluates from virus-treated stromata fluctuated considerably in samples obtained at various intervals during prolonged treatment.
5. Similar fluctuations in the titer of anti-Rh inhibitor in samples of eluates from periodate-treated stromata occurred only for a short time after treatment was begun, no inhibition being demonstrable in later samples.
6. Both titer and the fluctuations of inhibitor in eluates from mumps-treated stromata were affected by the stromata-virus ratio and by pH.
7. Fluctuations in the titer of anti-Rh inhibitor were correlated with fluctuations in the viral hemagglutinin titers of eluates.
8. Fluctuations in the inhibitor titer of virus-cell eluates were abolished by addition of antimumps serum and by inactivation of virus by heat. The subsequent addition of living virus to heated eluates was followed by the reappearance of the characteristic fluctuations of inhibitor titer.
9. The anti-Rh inhibitor in both types of eluates was tentatively identified as Rh0(D) antigen chiefly on the basis of its serologic specificity.
10. It was proposed that antigen existed in different forms in the two eluates. A carbohydrate complex having a dual antigen-receptor function was postulated for the virus cell eluate.
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