Abstract
Chick embryo fibroblasts (CEF) and hamster BHK21 cells transformed by the Schmidt‐Ruppin strain of Rous sarcoma virus (SR‐RSV) release into the culture medium a factor or factors which enhance 2‐ to 7‐fold the formation of transformed foci by chick embryo fibroblasts infected with the Bryan strain of RSV (B‐RSV). The factor(s) also increase the number of foci failing to revert to normal phenotype at restrictive temperature (41° C) in cultures infected with a temperature‐sensitive mutant (FU‐19) of SR‐RSV which is defective for transformation. The factor (s) is produced also by BHK21 cells transformed by other tumor viruses and by BHK21 cells passaged for a long time, but not by normal CEF, CEF transformed by B‐RSV, CEF infected by FU‐19 at 41° C, normal hamster embryo fibroblasts, established but density‐inhibited mouse fibroblasts, or BHK21 cells of early passages. The relative enhancement of the number of B‐RSV foci can be more than 100‐fold when the medium contains fetal calf serum which suppresses focus formation in controls. The focus‐enhacing factor (s) appears to act after infection and has been termed, operationally, transformation‐enhancing factor (s) or TEF. The factor produced by RS2/3 cells which enhances the formation of B‐RSV foci is non‐dialyzable and thermolabile, and is presumably a protein. Its molecular weight is between 10^6^ and 2 × 10^5^ daltons.