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Since Zilber and Kriukoval and Svet-Moldavsky' demonstrated that some strains of Rous sarcoma virus (RSV) are capable of inducing hemorrhagic cysts or sarcomas in newborn rats, numerous attempts have been made to induce tumors by RSV in various species of mammals.3-9 One of the remarkable aspects revealed by these investigations is the strain differences in RSV for this capacity.6-9 Certain strains, such as the Schmidt-Ruppin strain, are active, while others, such as the Bryan strain, are generally inactive in mammals. The cause of such strain differences has not been elucidated. Our previous studies have shown that the Bryan high-titer strain of RSV is a defective virus which cannot reproduce without the help of any one of the avian leukosis viruses.'0 The defectiveness derives from the inability of this strain of RSV to induce the synthesis of its own viral envelope."I An essential role played by the helper virus is to provide the envelope to the RSV genome, whose replication occurs in the infected cells without the aid of helper virus. Thus, several properties of RSV which presumably depend in some way on the character of the viral envelope are controlled by the helper virus used to activate the RSV.11-13 These properties include the antigenicity, the sensitivity to the interference induced by the helper virus, and the host range among genetically different chick embryos. These findings raised the question whether certain strains of RSV are active in mammals because they have a special envelope or because they have a special genome. Developments in the ways of changing the RSV envelope without changing the genome and of discriminating among viruses with different envelopes by their phenotypic properties have made it possible to investigate this problem. The present communication provides evidence that the viral envelope is the main determining factor in the tumor induction of RSV in mammals. Materials and Methods-Notation: It is now possible to obtain variants of Bryan high-titer or Schmidt-Ruppin RSV by the use of various helper viruses to provide different coats. However, these RSV variants differ only in the character of the envelope; their genome remains the same.13 To distinguish these phenotypic variants of RSV, a notation has been introduced giving the respective helper virus in parentheses after RSV."1 To distinguish the different strains of RSV where the viral genomes are different, the abbreviation RSV will be preceded by the initials of the strain name.'4 For example, BH-RSV(RAV-2) and SR-RSV(RAV-1) refer, respectively, to the Bryan high-titer strain of RSV whose envelope-dependent characters are controlled by Rous associated virus-2, or RAV-2, and to the Schmidt-Ruppin RSV whose envelope-dependent characters are controlled by Rous associated virus-i, or RAV-1. Viruses: The preparations of RAV-1, RAV-2, BH-RSV(RAV-1), and BH-RSV(RAV-2) have already been described."3 1" The helper viruses were assayed by the capacity to induce interference to their cognate BH-RSV." The original stock of SR-RSV obtained from Dr. H. Rubin, who had received it from Dr. Ahlstrdm, was purified by the single focus isolation.16 Two properties, the nondefectiveness'4' 16, 17 and the morphology of foci of transformed cells, were used to distinguish the Schmidt-Ruppin strain from Bryan strain of RSV. These properties of RSV were proved to be under the control of RSV genome and were not affected by altering viral envelopes with those of various helper viruses.14, 16

Determining factor in the capacity of Rous sarcoma virus to induce tumors in mammals.