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Abstract
The C-C chemokine receptor 5 (CCR5) is expressed on potential human immunodeficiency
virus (HIV) target cells and serves as the predominant co-receptor for viral entry
during initial transmission and through the early stages of infection. A homozygous
Δ32 mutation in the CCR5 gene prevents CCR5 cell surface expression and thus confers
resistance to infection with CCR5-tropic HIV strains. Transplantation of hematopoietic
stem cells from a CCR5Δ32/Δ32 donor was previously successful in eliminating HIV from
the recipient's immune system, suggesting that targeted CCR5 disruption can lead to
an HIV cure. Therefore, intense work is currently being carried out on CCR5 gene-editing
tools to develop curative HIV therapy. Here, we review the natural function of CCR5,
the progress made on CCR5 gene editing to date and discuss the current limitations.