Avian sarcoma viruses of subgroup C efficiently infect and transform d
uck cells, but their replication is impeded. Nevertheless, after prolo
nged passage of the Prague strain of Rous sarcoma virus subgroup C (Pr
-RSV-C) in duck embryo fibroblasts the virus becomes adapted to the ne
w host and regains the ability to replicate as efficiently as in its o
riginal 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 (tr
ansformed with the adapted virus) and completely sequenced. Comparativ
e 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 re
sponsible 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 ho
st range. The multiple changes found in the new variant are probably d
ue to homologous recombinations between the corresponding regions of t
he endogenous chicken retroviruses.