HIV Targeting and Making Genetic Alterations in Embryos

As a pre-requisite of HIV binding to CD4 T cells, CCR5 is instrumental in ensuring HIV infection of the host. A naturally occurring mutation in the CCR5 gene is termed “delta 32” or CCR5Δ32. The deletion of the 32 base pair fragment in the CCR5 gene considerably reduces risks of HIV infection as a result of disabled CCR5 co-receptors on the surface of CD4 T lymphocytes, the very target of HIV. In an attempt to mimic CCR5Δ32, Dr. He Jiankui used the CRISPR/Cas9 gene editing tool and edited wild-type CCR5 in two human embryos that subsequently gave rise to two baby girls.³⁴ The scientist described that some (but not all) CCR5 tested in the two baby girls harbored CCR5Δ32, indicating that the baby girls carry a mixture of wild-type CCR5 and mutant CCR5Δ32. Putting aside whether residual wild-type CCR5 would enable successful HIV invasion and infection, the very fact of making genetic alterations in embryos is the source of the outrage from the scientific community. To be clear:

Intriguingly, even though embryonic or germline editing is officially prohibited, the finer print of the guidelines reveals that the prohibition of embryonic/germline gene editing is not supported by government-funded research, suggesting that there are, at least not at this time, any laws governing against such research sponsored by private findings. At this point, the issue of whether or not clearly stated laws against embryonic/germline gene alterations by any type of funding remains controversial and contentious.