I don’t believe so. I looked into it a bit more, and it looks like homozygous variant carriers are more susceptible to other types of infection (West Nile is specifically cited), but I don’t see anything showing the variant causes issues with CCR5s other critical functions. I do think a knockout is probably a bad idea based on further reading, but modification seems like a promising path.
I meant a compensatory mutation on another receptor or protein besides CD163. I kinda meant it rhetorically. It's not an easy thing to answer.