Experimental analysis reveals CRISPR can target HIV in CD4+ T cells, suggesting a breakthrough in treatment.
The human immunodeficiency virus (HIV) devastated the world in the 1980s in a global epidemic, killing millions over the years. Despite the epidemic initiating over 40 years ago, there is no cure apart from some rigorous treatments that reduce HIV spread across the human body. However, the recent advent of clustered regularly interspaced short palindromic repeats (CRISPRs) as a modifiable gene-editing technology provides a permanent solution to a currently incurable disease. Editing the gene expressing the receptor CD4 and one of the co-receptors, CXCR4 or CCR5, prevents expression of these receptors, thus removing all possible options for HIV to bind and inject its genetic material in a CD4+ T cell. After injecting a specialized lentiviral vector compartment containing a Cas9 enzyme, single-guide RNA, and ribonucleoprotein, the paper details a specific way of using electroporation, a method utilizing electrical currents to open temporary pores in the cell membrane, on specific locations depending on the age of the patient. This allows for smoother transport of the gene editing lentiviral vector. These components will be transferred through the nuclear membrane as well with the nuclear localization signals facilitating its entrance into the nucleus, after which the sgRNA guides the Cas9 to the point of cleavage, after which the system self-degrades almost immediately to ensure there is no potential random insertion or deletion caused by long-term Cas9 presence.
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Bhatia et al. (2025) studied this question.
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