It has also been observed that 20% of the Caucasian population possess a mutation, called CCR5-Δ32 (frequency of 0.0808 for homozygous allele), that prevents the CCR5 chemokine receptor protein, which is the main means of viral access into the cell, from being expressed on the surface of their CD4+ T-cells. Individuals who are homozygous for this mutation are immune to HIV strains that use the CCR5 receptor to access the cell, while those that are heterozygous for this mutation have been found to reduce plasma viral load and delay progression of AIDS.Lai, Y. CCR5-targeted hematopoietic stem cell gene approaches for HIV disease: Current progress and future prospects Current Stem Cell Research and Therapy, 2012; 7 (4), pp. 310-317. By combining these facts, researchers have proposed a novel method of treatment for HIV. This method attempts to treat the infection by disrupting the CCR5 gene, such as introducing the CCR5-Δ32 mutation using a recombinant adenoviral vector or forcing DNA repair by nonhomologous end joining, which is prone to error and results in a non-functional gene. As a consequence, resulting in the expression of nonfunctional CCR5 co-receptors on CD4+ T cells, providing immunity against infection.
