These data are reminiscent of studies with HIV-1 ADA where removal of an N-linked glycosylation site at the base of the V1V2 stem (N197) facilitated CD4-independent infection of canine cells through CCR5 [12], an effect that was postulated to be mediated by repositioning of the V1V2 loops and exposure of the CCR5 binding site [12]. This evidence concerns the gene ADA and infection.