Human immunodeficiency virus (HIV) can be transmitted by infected individuals through sexual fluids, blood, and breast milk. It functions to weaken the immune system by targeting healthy CD4 cells and in turn, impedes the body’s ability to fight minor infections. In order to infect the host, the virus must first bind to a CD4 receptor followed by binding of a co-receptor; either CCR5 or CXCR4. A specific mutation to the CCR5 receptor at position D32, results in a 32 base pair deletion and hypothesized to inhibit expression of the CCR5 receptor on the cell surface of T-cells. It has been found that individuals who are homozygous for D32 mutation are resistant to HIV infection whereas those heterozygous for the mutation exhibit a slower onset of symptoms. We used the gene editing tool CRISPR/Cas9 to target and cut specific sequences on the CCR5 gene that are believed to prevent receptor presentation of the surface of T-cells. We expect that only HIV that can utilize CXCR4 as a co-receptor would be able to infect CCR5 knock out cells.