Using dual CRISPR gene-editing therapy, researchers were able to silence or remove two distinct genes from HIV-infected humanized mice.
About 60% of the models had no detectable virus after the researchers used this method in conjunction with a long-acting form of antiretroviral therapy, which was a significant increase from the 29% reported in 2019.
The CRISPR gene-editing therapy
Dr. Khalili and his co-investigator, Rafal Kaminski, Ph.D., Assistant Professor at the Center for Neurovirology and Gene Editing at the Katz School of Medicine, combined their knowledge of CRISPR gene-editing technology for targeting HIV-1 with a therapeutic strategy called long-acting slow-effective release (LASER) antiretroviral therapy (ART).
Which was developed by Dr. Gendelman and Benson Edagwa, Ph. With LASER ART, HIV replication can be kept at low levels for extended periods of time, reducing the need for ART dosing.
In LASER-ART mice, HIV was eradicated, but tissue reservoirs could reactivate the virus. If antiretroviral therapy (ART) is interrupted, this is similar to rebound infection in humans.
Antiretroviral medications cannot reach HIV in tissue reservoirs when it inserts their DNA into the host cell’s genome. Thus, ART discontinuation causes HIV replication and AIDS.
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Role of CCR5 in Facilitating HIV
Dr. Khalili and his team are working on a novel, dual approach to eradicate HIV from the animal model for good, with the goal of preventing re-infection.
They devised a less complicated and more useful method, including intravenous administration of the CRISPR gene-editing molecule, for rendering CCR5 functionally inactive.
When the Temple constructions were combined and given to humanized LASER-ART mice, Dr. Gendelman’s team found that 58% of the infected animals experienced viral suppression, reconstitution of human T-cells, and elimination of replicating HIV-1.
The results lend credence to the theory that CCR5 plays a significant role in HIV facilitation.