Possibly useful HIV treatment by modifing bone marrow

HIV needs 2 specific receptors on T-cells to enter them and multiply. One is CD4 and other 2 are CCR5 and CXCR4. Those last 2 are receptors to chemokines that regulate movements of white blood cells. If those 2 are mutated enough then HIV can't enter them and it seems people with these mutations don't get infected with HIV without having serious health problems.
For example if all human ccr5 receptor genes have ccr5Δ32 mutation (32 base pairs missing) then they don't produce CCR5 and their T-cells don't get infected with R-5 (CCR5-tropic) HIV strain and those who have one mutated copy in one of the chromosome produce less CCR5 and tend to live longer after HIV infections. If HIV type uses CXCR4 then this  previous mutation would not protect against infection.
Authors of this study decided to use proteins (zinc-finger nuclease) that break DNA from certain places so cxcr4 genes would mutate due to errors that happen when DNA parts rejoin. Using these proteins seemed to protect T-cells from HIV strains (X-4 tropic) that used CXCR4 for entering T-cells. If CCR5 and CXCR4 both got mutated enough then the protective effects improved. 
Cells grown outside body seemed to tolerate these added mutations and kept multiplying.

Above illustration shows how much HIV affected different T-cells and how many were alive in different days. NTD is normal T-cell. R5ZFN is zinc finger nuclease that damages CCR5 and X4ZFN mutates CXCR4. X4ZFN seemed most protective against the 3 HIV strains they tested on T-cells without much cell death after HIV infection.
In one case a HIV positive patient got bone marrow due to leukemia and donor had ccr5Δ32 gene versions. Authors also noted that they know about humans with large CXCR4 mutations and that CXCR4 is involved in development of brain and cardiovascular system so mutation of that gene are probably deadly for fetus although mutations with ZFN in adults seem tolerable. As blood cells are produced in marrow it also caused production of mutated T-cells. After transplantation his HIV viral load remained undetectable even 3 years after transplantation.
Authors said it could be first "HIV cure" although transplantation of tissue from other person means patient has to take immune weakening drugs that may cause more serious infections and tumors. Also such mutations are rare for transplantations to all HIV positive patients. One alternative they offered was to use ZFN proteins to produce marrow with patients own cells that would produce HIV resistant T-cells.

My comment: if CXCR4 are needed to grow cardiovascular system and brain then mutations in them could make having children impossible if patients CXCR4 genes would get mutated in all their cells but authors wrote mostly about removing tissue, mutating it and re-transplanting.