The change that has been studied is a naturally-occurring 32 base pair deletion of the CCR5 gene (see https://www.google.com/search?q=ccr5+delta+32 https://www.

The change that has been studied is a naturally-occurring 32 base pair deletion of the CCR5 gene (see https://www.google.com/search?q=ccr5+delta+32 https://www.google.com/search?q=ccr5+delta+32). In the literature, this allele is called CCR5-Δ32, and it modifies the expression of the CCR5 protein by, among other things, eliminating the receptor used by some HIV strains. He Jiankui intended to use CRISPR to effect CCR5-Δ32, but didn't succeed; instead, his use of CRISPR made other, never-studied-before mutations to the CCR5 gene. Will those mutations result in a CCR5 protein which confers HIV resistance? Probably, at least to some strains, since as far as we know, the full CCR5 gene is needed for an HIV-compatible receptor on the CCR5 protein. Will they have other effects? What is their safety profile? These mutations have never been studied before, so no one knows. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6813942/#__p275 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6813942/#__p275 for more on this.