Our finding of attenuation of the copY mutant in vivo may be related to exposure of the bacteria to Cu or Zn during infection; however, ΔcopY GBS overexpresses copA-copZ (so should be more resistant to Cu) [20]; additionally, we did not measure tissue levels of metal ions in this study pointing to a need to further characterise the basis of the attenuation of ΔcopY GBS in vivo. This evidence concerns the gene COPA and infection.