I think yes from the article?
> CRISPR does the cutting only, and you rely on cell repair mechanisms to mend the parts together again
But in this case, all we need is the cutting right because we don't care if the HIV survives the interaction.
Agreed on the quote
In the "what could possibly go wrong" scenario, if it survive this drives the virus for mutantion.
HIV is a retrovirus, it inserts itself into the hosts's genome, making dormancy easier.
"The major reservoirs for HIV in the CNS are in the microglia, perivascular macrophages, and to a lesser extent, astrocytes" https://pubmed.ncbi.nlm.nih.gov/27873219/
While CRISPR is often used in cultured cells (eg for CAR T therapies) there are CRISPR therapeutics in live human patients today in phase 3 trials for sickle cell disease (among other indications).
https://doi.org/10.1056/nejmoa2031054
> Approximately 80% of the alleles at this locus were modified, with no evidence of off-target editing. After undergoing myeloablation, two patients - one with TDT and the other with SCD - received autologous CD34+ cells edited with CRISPR-Cas9 targeting the same BCL11A enhancer.
Similar (not the same) things have already been done multiple times for HIV patients who had to have their bone marrow destroyed for other reasons, generally leukemia (Düsseldorf Patient, Geneva Patient, London Patient, etc). They received transplants from donors that had mutations in CCR5, which prevents HIV. But you can't cure 40 million people living with HIV that way.
This therapy is extremely involved, expensive, and it also impacts the health of the patient (e.g. their entire immune memory is reset, they have to redo all their vaccinations). You don't destroy the bone marrow of someone due to no reason. Them requiring regular blood transfusions is a good reason, but them having to take antiretroviral drugs once per day is generally not seen as one.
The paper of this thread is about a single injection that does these CRISPR edits while inside the patient, without involving destruction of the bone marrow.
Also, the reservoir that makes HIV so tricky is in immune cells that are in a sleep state and only wake up every now and then: can the viral vector reach those?
Also important quote from the paper:
> The study was not designed to test the effect on the intact viral reservoir as EBT-001 was given when the viral reservoir was not stable and there was still active viral replication. Additionally, as animals were maintained on ART, we did not test the ability of EBT-001 to extend time to viral rebound or eliminate viral reactivation after an analytical treatment interruption.