In particular, simultaneous disruption of the HIV receptors CXCR4 and CCR5, either in primary human T-cells via cytosine base editors or in primary T-cells, and CD34+ HSPCs via adenine editors efficiently disrupted CXCR4 and CCR5 expression thus protecting from CXCR4- and CCR5-tropic viral infections [76]. The gene discussed is CCR5; the disease is viral infectious disease.