Selective infection of cultured cells by HS-binding mutants. (Left panel) Normal cell lines, such as RD-A, show low cell surface expression of SCARB2 and high expression of HS. Therefore, the infection efficiency of wild-type HS-nonbinding mutants is low. By contrast, a small number of HS-binding mutants emerge during replication and efficiently infect cells through HS; thus, HS-binding mutants become dominant. (Right panel) In RD-∆EXT1+hSCARB2 cells, selective infection by HS-binding mutants is less likely to occur because the expression of SCARB2 and HS, responsible for such infection bias, is optimized.