Sangamo BioSciences Presents Data at ICAAC Demonstrating 'In Vivo' Protection Against HIV Infection by CCR5-ZFN T...(ic ZFNs resulted in the generation of an...)

Date:10/28/2008

ic ZFNs resulted in the generation of an HIV-resistant population of primary human T-cells by the permanent genetic modification of the CCR5 gene. These ZFN-modified CD4 T-cells expanded stably in HIV-infected cultures for several weeks and appeared to behave identically to untreated T-cells except that they were resistant to infection by HIV. ZFN treated primary CD4 T-cells and transformed CD4 cell lines resisted infection with R5-tropic HIV (virus that uses the CCR5 co-receptor to enter cells), resulting in enrichment of ZFN-generated CCR5-disrupted cells in the population upon exposure to virus. Importantly, in the presence of HIV, ZFN-modified CD4 T-cells also preferentially expanded in a mouse model. The modified cells were infused into mice that lack a normal immune system and thus do not reject human cells. After 33 days, the mice were sacrificed and analyzed for the presence of ZFN-modified cells. Researchers determined that ZFN-modified cells engrafted normally in the mouse and that the proportion of modified cells present at the end of the experiment was greater than two to three fold higher in mice in the presence of HIV infection (p=0.008). It was also determined that 50 days after infection, mice given the ZFN-modified cells had increased numbers of CD4 cells and a statistically significant seven-fold reduction in viral load in their peripheral blood (P<0.001) compared to mice given control cells. A high level of specificity of the CCR5-ZFNs for their target site was demonstrated by immunochemistry and direct genomic sequence analysis of ZFN-treated human CD4 T-cells. These data suggest that, in the presence of HIV, the ZFN-modified cells have a selective advantage allowing them to evade infection and destruction leaving them able fight opportunistic infections and HIV itself.

In addition, Sangamo and its collaborators have demonstrated successful ZFN-modification of clinical-scale quantities of human CD4 T-cells and that these modified cells exh
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