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.
Highlights
CD4 and a co-receptor, predominantly the chemokine receptor CCR5
HIV replication and mitigate the development of resistance. For this reason we have introduced a second element into its anti-HIV lentiviral vector construct
The “Berlin patient” showed that modulating CCR5 can lead to a functional cure of HIV
Summary
The entry of human immunodeficiency virus type 1 (HIV-1) into target cells requires both CD4 and a co-receptor, predominantly the chemokine receptor CCR5. A 32 base pair deletion in the CCR5 gene results in a truncated protein that is insufficient for HIV entry. CCR5-delta homozygosity provides natural protection against HIV infection without detrimental effects to the host, further commented on below [1]
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