Abstract
Ecotropic murine leukemia viruses, both N-tropic FN-2 (purified helper component of Friend leukemia virus) and B-tropic WNB-2 (purified WN1802B BALB/c-derived endogenous virus), were partially restricted in rat NRK cells. In NRK cells, they produced obscure small plaques at reduced efficiencies relative to their plaque-producing efficiencies in mouse SC-1 cells (10-fold for FN-2 and 100-fold for WNB-2). After three or four passages in NRK cells, the plaquing efficiencies of the viruses in NRK cells increased to levels close to their efficiencies in mouse cells, and the plaques in NRK cells became larger and clearer. The adaptation was more complete with FN-2 than with WNB-2. The adaptation was not due to simple selection of a virus in the FN-2 stock, but was host induced, as the viruses had been submitted to successive limiting dilutions in SC-1 cells before propagation in NRK cells. Possible commitment of xenotropic virus in the adaptation was excluded. The change was stable, even if the adapted viruses were propagated back into SC-1 cells. The NRK-adapted viruses were restricted in other rat cell lines of different origins, and the virus adapted in another rat cell line, RFL, was still restricted in NRK cells. The adaptation was mainly brought about by increased viral growth within the rat cells and not by an increased efficiency of viral penetration into the rat cells. This inversely suggests that the restriction of the ecotropic murine leukemia viruses in NRK cells was a mainly intracellular event. The mobilities of gp69/71 and p30 in sodium dodecyl sulfatepolyacrylamide gel electrophoresis remained unchanged after adaptation of FN-2 in NRK cells.