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Evidence Suggesting a Relationship between Polyoma Virus-induced Transplantation Antigen and Normal Embryonic Antigen¹

Department of Medical Microbiology, School of Medicine, Stanford University, Stanford, California and Stanford Research Institute, Menlo Park, California 94025

The polyoma virus-induced transplantation antigen (PYV-ITA) in embryonic hamster cells was investigated with rabbit antiserum. A spontaneously transformed, tumor-producing, embryonic hamster cell line (STF) that arose from the same noninbred animal stock as did the polyoma virus-transformed cells (PTF) was used as a control. An antigen present in the PTF cells, but not in the STF cells, was detected by rejection experiments in polyoma virus-immunized adult hamsters and by cytotoxicity with STF-absorbed, rabbit anti-PTF, rabbit serum. Evidence was demonstrated that the antibody activity did not reflect an isoantigenic difference between these two cell lines. The results strongly favored the probability that the antigen on the PTF cells was a polyoma virus-associated, cellular "tumor" antigen (PYV-ITA). However, it was shown to be also a component of normal embryonic hamster cells but was not detectable in the mature cells of the adult spleen or in embryonic mouse cells (3T3) transformed by polyoma virus. Furthermore, spleen cells from mature hamsters immunized with normal embryonic hamster cells were shown to be cytotoxic to the PTF cells.

These results suggest that the PYV-ITA may have been determined in part by an embryonic cellular gene, rather than altogether by a viral gene, and may be closely related to antigen existing in normal embryonic cells but not in either the STF cells or in spleen cells of the normal adult hamster. In view of these results, a hypothesis is presented to suggest a possible role of the virus in the induction of both the antigen and the transformed state.

¹ Supported in part by Contract No. PH 43-65-43 with the CCNSC of the National Cancer Institute, NIH, and by Training Grant No. AI 82, National Institutes of Allergy and Infectious Disease, USPHS.

² The work reported in this paper was submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy.

³ Present address: Department of Tumor Biology, Karolinska Institute, Stockholm 60, Sweden.

Received 11/20/67. Accepted 5/12/68.