Tumor-Induced Skin Heterogenization. II. Virus Causing the Phenomenon

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Abstract
Sarcoma K-237 of C57BL/6J mice contained a permanent skin-heterogenizing virus (SHV), which caused the same phenomenon of tissue incompatibility as the tumor itself. SHV was ether resistant and thermolabile; it could be specifically neutralized with C57BL/6J immune serum. Preliminary sedimentation data showed SHY particles were very small. This evidence was confirmed partly by the discovery of two types of virions, 175 and 80 A in diameter, in an active fraction of the homogenate. Homogenates obtained from tumors of the 7th–22d passages contained SHV titers of 108–1012 heterogenization-producing doses per ml. However, those obtained from tumors of the 23d–27th passages contained SHV titers of 101–105. The state of heterogenization was maintained in infected mice from the 21st–240th day after inoculation. The behavior patterns of the virus in tumor cells were somewhat different from those of skin grafts. One may suppose that the virus in the skin is in some way integrated with the cells and passes from cell to cell by some unknown mechanism. Infectious virus was obtained from the skin homogenate only once after inoculation with tumor homogenate but never after skin graft infection. Nevertheless, each skin passage resulted in skin heterogenization. SHV persisted in the spleen of rejector mice in large amounts (titers 105–107) at least for 120 days after infecting grafting. The exchange skin grafting between rejector mice resulted in survival of transplants, though the skin from the same animals was rejected as usual by normal C57BL/6J recipients.

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