Role of 3′-end of viral genome in tumor heteroinduction by the avian sarcoma virus

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Abstract
Transformation defective virus was derived by restriction endonuclease cleavage from a clone of the avian sarcoma virus Schmidt‐Ruppin strain, strongly oncogenic for rats. The transfection experiments of chicken cells by digested proviral DNA gave rise to transformation defective virus. The td virus was possible to recover in vivo in chickens. The tumors obtained after a long latent period contained the sarcoma virus which was able to transform chicken cells in vitro and to induce tumors in chickens. All viruses, parental, td‐ and recovered were of D subgroup specificity. The tumor induction experiments in rats have shown that the recovery of viral genome deletion in td mutant by cellular sequences was not enough to regain the oncogenicity for rats. The results stressed the importance of 3‐end sequences of the virus genome, probably the sequences in C region for heteroinduction ability of the avian sarcoma virus.