Abstract
The multiplication of fowl-plague virus was much less sensitive to actinomycin D in chick cells infected with avian myeloblastosis virus and in hamster cells, transformed by Rous sarcoma virus than in comparable normal cultures. In addition, reproduction of fowl-plague virus was less effectively suppressed by u.v.-irradiation of cells carrying avian myeloblastosis or Rous sarcoma virus than of control cultures. These findings could indicate that avian myeloblastosis and Rous sarcoma viruses induce a function of host-cell DNA, whose products can be utilized in reproduction of fowl-plague virus.
* Present address: Imperial Cancer Research Fund, Lincoln's Inn Fields, London, W.C. 2