Abstract: Human immunodeficiency virus type 1 (HIV-1) infection of target cells requires CD4 and a co-receptor, predominantly the chemokine receptor CCR5. CCR5-delta32 homozygosity results in a truncated protein providing natural protection against HIV infection—this without detrimental effects to the host—and transplantation of CCR5-delta32 stem cells in a patient with HIV (“Berlin patient”) achieved viral eradication. As a more feasible approach gene-modification strategies are being developed to engineer cellular resistance to HIV using autologous cells. We have developed a dual therapeutic anti-HIV lentiviral vector (LVsh5/C46) that down-regulates CCR5 and inhibits HIV-1 fusion via cell surface expression of the gp41-derived peptide, C46. This construct, effective against multiple strains of both R5- and X4-tropic HIV-1, is being tested in Phase I/II trials by engineering HIV-resistant hematopoietic cells.
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Burke, B.P.; Boyd, M.P.; Impey, H.; Breton, L.R.; Bartlett, J.S.; Symonds, G.P.; Hütter, G. CCR5 as a Natural and Modulated Target for Inhibition of HIV. Viruses 2014, 6, 54-68.
Burke BP, Boyd MP, Impey H, Breton LR, Bartlett JS, Symonds GP, Hütter G. CCR5 as a Natural and Modulated Target for Inhibition of HIV. Viruses. 2014; 6(1):54-68.
Burke, Bryan P.; Boyd, Maureen P.; Impey, Helen; Breton, Louis R.; Bartlett, Jeffrey S.; Symonds, Geoff P.; Hütter, Gero. 2014. "CCR5 as a Natural and Modulated Target for Inhibition of HIV." Viruses 6, no. 1: 54-68.