The present study also considered whether altered glycosylation could explain why two cells expressing the same dCAT-1 receptor, M. dunni and FerrD2, produce syncytia in response to different viruses. As shown by the inhibitor results, however, while N-glycans contribute to the restriction of MoMLV entry into M. dunni cells, comparisons of ferret transfectants expressing the dCAT-1 or dCAT-1-g receptor variants produced no evidence that N-glycans modulate virus infectivity or virus-induced cytopathicity in the MA139 cells.