The fact that these two viruses are only cytopathic in M. dunni cells suggests involvement of the receptor-virus interaction for two reasons. First, the amino acid residue that is modified in both viruses has been identified as one of the critical amino acids forming the receptor binding site [3, 4] . Second, M. dunni cells differ from other mouse cells in their resistance to MoMLV [5] , and these cells are known to carry a modified CAT-1 receptor (dCAT-1). The dCAT-1 gene of M. dunni cells differs from the prototypical CAT-1 gene of the laboratory mouse (mCAT-1) in that the third extracellular loop that contains the virus binding region has a substitution (I214V) as well as an inserted glycine after Y235, a residue critical for receptor function [6] (Fig. 1A) .