Mechanism of Resistance to Mammary Tumor Development in C57BL and I Strains of Mice. II. Inherent Differences Between the Two Strains2

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Abstract
Experiments were designed to follow the fate of the mammary tumor virus (MTV) and the host reactions to MTV and associated antigens in C57BL/Crgl (hereafter referred to as C57) and I/Crgl (I) strains of mice. Introduction of C3H MTV into C57 and I mice resulted only in occasional milk transmission of MTV by these mice. However, (C57 × I)F1 (F1) mice, exposed to MTV, could transmit virus serially in successive passages. After being naturally or artificially introduced into C57, I, and FI mice, MTV quickly disappeared in all 3 groups; thereafter, it remained undetectable in blood cells and hematopoietic tissues of C57 mice. MTV activity, however, reappeared rarely in blood cells and spleens of young I mice; such reappearance was always observed in blood cells of FI mice beginning at about 3–4 weeks of age. Production of blood cell-associated MTV and noduligenesis failed to occur, even under strong hormonal stimulation, in C57 mice implanted with C57 mammary nodular outgrowths capable of continuous production of MTV B particles. Noduligenesis did occur in F1 mice implanted with the same C57 nodular outgrowths. Transplanted I nodule outgrowths usually failed to establish or induce nodules in I hosts. After natural infection with MTV or after immunization with MTV-containing antigens, I, but not C57, mice developed virus-neutralizing antibodies. Few of the I nodules, when transplanted into untreated I hosts, survived and produced hyperactive outgrowths. However, a higher percentage of I nodules, when transplanted into I hosts tr.eated with rabbit antimouse thymocyte serum, could produce hyperactive outgrowths. The implications of these results are discussed

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