THE DEFECTIVENESS OF ROUS SARCOMA VIRUS

Publisher Website
Google Scholar
Abstract
In an attempt to obtain the high titer strain of RSV free of RAV, isolated foci of transformed cells were produced by infecting chick embryo cultures with very high dilutions of the RSV stock. Agar, containing antibody to RAV, was added to the cultures to minimize the spread of RAV. The transformed cells were added to uninfected chick embryo cells and retained their altered morphology through repeated serial transfers. Most of the foci maintained in this way yielded no detectable virus. In every such case, however, RSV production could be elicited by adding RAV or any one of several other avian tumor viruses. A high proportion, if not all, of the transformed cells produced RSV upon superinfection with RAV, even when they had undergone well over 20 divisions in the absence of virus production. A minority of the foci produced RSV spontaneously upon transfer and in every such case RAV was also produced. The proportion of foci producing RSV and RAV spontaneously was matched by the proportion of interfocal areas of normal cells which produced RAV alone. This indicated that RAV from the inoculum had infected cells at random and that the "spontaneous" production of RSV by transformed cells was due to the delayed spread of RAV following the removal of antiserum. It is concluded that the high titer strain of RSV is defective since it cannot generate the production of new infectious virus unless a helper virus such as RAV is multiplying in the same cell. By contrast, however, the ability to cause the malignant transformation is expressed continuously, and consequently does not require the production of mature virus. Both the potential for virus production and the ability to transform cells are perpetuated in a cell line by hereditary transmission.