Mishma:
It escaped my attention on the Zinc Finger Protease (nuclease) "stacking" posts that the gene cassette they use includes the innate pattern recognition receptors TRIM5 alpha, which recognizes the capsid of HIV within the cells cytoplasm and APOBEC3G, which interferes with viral replication. CCR5, which is edited out in this system, can also be considered an innate pattern recognition receptor (Yes it normally binds a chemokine but it's structure doesn't change over the course of the immune response) as well as one of the HIVs co-receptors required for entry.
Stopping HIV Using a Cocktail of Genes Rather than Drugs: An amfAR Grantee Update
By Jeffrey Laurence, M.D. Published Friday, February 15, 2013
Dr. Matthew Porteus
The headline in The Huffington Post heralded this new amfAR-funded work by stating that, “HIV-resistant cells created by Stanford researchers could protect patients from AIDS.” An ABC News blog further declared that, “Genetically modified cells could prevent death from HIV/AIDS, study finds.” And what led to all this promise and excitement? amfAR grantees Dr. Matthew Porteus, working in the Department of Pediatrics at Stanford University, and Sara Sawyer at the University of Texas, have worked with colleagues to create, in the test tube, genetically modified human T cells resistant to HIV infection.
Porteus, Sawyer and colleagues took a lead from prior amfAR-funded research into so-called “restriction factors,” or normal cellular genes that have the capacity to limit the growth of HIV. Utilizing a novel and complex gene strategy based on enzymes that can cut into a host’s DNA, they were able to insert such factors—including APOBEC3G and TRIM5α—into a host gene, CCR5, disrupting that gene in the process. CCR5 normally codes for a critical receptor, or door, by which most strains of HIV enter a cell.
- See more at: http://www.amfar.org/Stopping-HIV-Using-a-Cocktail-of-Genes-Rather-than-Drugs/?msource=1302enews#sthash.W8D87keH.dpuf