Observations suggest that a cure strategy for HIV-1 infection should include methods that directly eliminate the proviral genome from the majority of HIV-1-positive cells, including CD4+ T-cells, and protect cells from future infection, with little or no harm to the host. The clustered, regularly-interspaced, short palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9) nuclease has wide utility for genome editing in a broad range of organisms including yeast,Drosophila, zebrafish, C. elegans, and mice, and has been applied in a broad range of in vivo and in vitro studies toward human diseases^{20,21,22,23,24}.

Recently we modified the CRISPR/Cas9 system to enable recognition of specific DNA sequences positioned within the HIV-1 promoter spanning the 5′ long terminal sequence (LTR)^25,26. Using this modified system, we now demonstrate excision of integrated copies of the proviral DNA fragment from a latently HIV-1-infected human T-lymphoid cell line, completely eliminating HDAC inhibition-elicited viral production. Results of whole-genome sequencing and comprehensive bioinformatic analysis ruled out any genotoxicity to host cell DNA. Further, we found that lentivirally-delivered CRISPR/Cas9 reduces viral replication upon HIV-1 infection of primary cultured CD4+ T-cells. The results point toward this approach as a promising potential therapeutic avenue to eradicating HIV-1 from T reservoir cells of host patients, to prevent AIDS re-emergence.

http://www.nature.com/articles/srep22555

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