Avian sarcoma viruses of subgroup C efficiently infect and transform duck cells, but their replication is impeded. Nevertheless, after prolonged passage of the Prague strain of Rous sarcoma virus subgroup C (Pr-RSV-C) in duck embryo fibroblasts the virus becomes adapted to the new host and regains the ability to replicate as efficiently as in its original host-the chicken cells. After 30 passages in chicken cells the provirus of Pr-RSV-C was cloned in a genome library of duck cells (transformed with the adapted virus) and completely sequenced. Comparative analysis of the nucleotide sequences of the adapted (daPr-RSV-C) and original (Pr-RSV-C) virus genomes revealed a number of characteristic differences, mainly in the gp85-coding domain of gene env which is responsible for the recognition of the appropriate cell surface receptor. Changes in the long terminal repeat (LTR) and the src gene may also contribute to the processes involved in the broadening of the virus host range. The multiple changes found in the new variant are probably due to homologous recombinations between the corresponding regions of the endogenous chicken retroviruses.