Induction of Simian Virus 40-specific Tumour Rejection by the Ad2+ND2 Hybrid Virus

Pediatric Oncology Branch and Macromolecular Biology Section, National Cancer Institute, and Laboratory of Experimental Pathology, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Md. 20205, U.S.A. Immunization of BALB/c mice with Ad2 + ND...

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Veröffentlicht in:Journal of general virology 1979-08, Vol.44 (2), p.287-296
Hauptverfasser: Jay, Gilbert, Jay, Francis T, Chang, Chungming, Levine, Arthur S, Friedman, Robert M
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Sprache:eng
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Zusammenfassung:Pediatric Oncology Branch and Macromolecular Biology Section, National Cancer Institute, and Laboratory of Experimental Pathology, National Institute of Arthritis, Metabolism and Digestive Diseases, National Institutes of Health, Bethesda, Md. 20205, U.S.A. Immunization of BALB/c mice with Ad2 + ND 2 , a non-defective hybrid virus containing about half of the early region of simian virus 40 (SV40) DNA covalently integrated into the human adenovirus 2 (Ad2) genome, can confer protection against subsequent challenge by syngeneic SV40 tumour cells. Analysis of subcellular fractions from Ad2 + ND 2 -infected cells shows a close correlation between the tumour rejection activity and the presence of the two SV40-specific proteins induced by this hybrid virus. These two proteins, with mol. wt. of 56000 (56K) and 42000 (42K), can be specifically immunoprecipitated using sera obtained from hamsters bearing SV40-induced tumours. Such immunoprecipitates, which contain no detectable contaminating components as determined by polyacrylamide gel electrophoresis, can efficiently immunize mice against SV40 tumour challenge, suggesting that the 56K and 42K proteins are directly responsible for the induction of tumour rejection. Moreover, we have found, by immunoprecipitation, a novel antigen in SV40-transformed BALB/c cells, also of 56000 mol. wt.; possibly, this 56K protein is responsible for induction of transplantation immunity in SV40-transformed cells. Received 24 August 1978; accepted 12 January 1979.
ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-44-2-287