The first week of May 2017 has been an historical one in the science community and more specifically in the closely followed HIV curing research. A study that has been ongoing for a while now was able in its latest stage to ensure the complete stoppage of replication and propagation of the virus by targeting its DNA through a process called gene editing.

What makes this achievement particularly remarkable is that it involved human immune cells that have been transplanted into mice, making it a very crucial step in the right direction, that of clinical trials on human subjects.

The revolutionary gene-editing technique called CRISPR/Cas9 was first patented to an MIT researcher in 2014 and has already been a huge part of some of the most significant studies of the last 3 years. In this experiment, the process was applied to mice at different stages of the disease and was successfully able to cut off HIV1 DNA from T cell genomes. It works by targeting specific parts of DNA inside a given cell with a protein that will actively make changes to these sections in a predetermined way.

Early last year, the same team was able to demonstrate that CRISPR/Cas9 can effectively eliminate HIV from the genome of every tissue of the affected subject’s body. However, they went even further in this study and proved that the same technique can also be effective with several other variations of the disease. Two of these variations were representative of both acute and latent infections in human cells, but the third involved literally injecting human immune cells into the mice before transplanting them with a chronic version of the HIV-1 virus.

This is extremely promising since one of the biggest challenges of dealing with HIV is that the chronic version of the virus can lay dormant for a while, essentially hiding from any therapy or destruction attempts, then suddenly become active again. However, this new study concluded that the chronic version can also be eliminated with gene-editing.

The next step will be to replicate the study in primates which offer a closer model to the human infection than mice do.


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