VLDLR and infection: We next tested whether naturally occurring polymorphisms on the E2–E1 glycoproteins in site 1 (L149Q or R224K) or site 2 (K181E or Q214R) explain why previously examined lineage B strains do not bind VLDLR or ApoER2 (Figure S8B).15 The site 2 K181E or Q214R substitutions when individually introduced into McMillan RVPs abolished infection of K562 cells expressing VLDLR, suggesting that K181 and Q214 are required for VLDLR binding by McMillan.