Minimally these data indicate that the uracilation phenotype is independent of whether the virus uses the CCR5 or CXCR4 co-receptors, but we cannot exclude that in vivo exposure of AM to different growth factors, cytokines or chemokines might influence the uracilation phenotype and infection kinetics as we have observed previously with varying the in vitro protocol for M-CSF treatment [31]. This evidence concerns the gene CXCR4 and infection.