Immunosuppressive Effects of Friend and Rauscher Leukemia Disease Viruses on Cellular and Humoral Antibody Formation2

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Abstract
Infection of mice with either Rauscher or Friend viruses, which induce leukemia-like disease, markedly interfered with antibody production on the cellular level, after immunization with sheep red blood cells (S-RBC), as detected by a localized hemolytic plaque assay for 19S and 7S antibody-forming cells. Cellular immunodepression was noted quite early and throughout the period after immunization when control animals were responding well with antibody formation. Mice simultaneously infected with virus and given injections of S-RBC had a slightly suppressed, immune, antibody-plaque response at the time of peak antibody formation 4 days later. Lengthening the interval between virus infection and S-RBC immunization resulted in greater immunosuppression. The number of antibody-forming cells after immunization was markedly depressed in virus-infected mice when calculated either as a ratio for the whole spleen or as the number of antibody-forming cells per million nucleated spleen lymphocytes. There was no compensatory increase of antibody-forming cells in lymph nodes and the thymus of virusinfected mice, as compared to noninfected controls. The appearance of antibody in the circulation decreased, as assayed by hemagglutination and hemolysis titrations of serum from virus-infected mice, compared to normal controls. Serum antibody suppression was not as marked as that observed on the cellular level. Virus-infected mice also had a suppressed secondary response when S-RBC were administered 10–15 days after the primary immunization. Appearance of both 7S and 19S antibody-forming cells was suppressed in the secondary-stimulated mice. Although immunodepression was detectable in all mice infected with virus before primary immunization, the most marked suppression was observed in animals with marked splenomegaly relatively late in the disease process. Total spleen weight and number of nucleated spleen cells increased after infection and were correlated with reduced numbers of antibody-forming cells. The results are discussed in relation to other studies indicating depressed immune responses to a number of antigens after infection of mice with a variety of tumor viruses or after treatment with carcinogens.

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