In a study published in the journal mBio, University of California, San Diego researchers found that if an RNA molecule essential in gene inhibition and activation - referred to as HEAL - is turned off or deleted using CRISPR-Cas9, HIV could be prevented from recurring, even when antiretroviral treatment is terminated.
The study focuses on latent HIV reservoirs, which are the cells of the body in which HIV is able to persist even when patients are undergoing antiretroviral therapy. If someone diagnosed with HIV does not take their antiretroviral medication, the amount of HIV in their body, called the viral load, will increase. Although antiretroviral drugs can suppress HIV viral loads, they cannot completely eliminate latent HIV reservoirs.
CRISPR-Cas9, or “Clustered Regularly Interspaced Palindromic Repeats,” is a technique that involves identifying the locations of mutations in genes and then using Cas9, an enzyme, to cut and remove unwanted portions of DNA along a gene sequence.
The researchers found that by genetically modifying long noncoding RNA (lncRNA) in immune cells called macrophages infected with HIV, they were able to prevent HIV recurrence in the immune cells. IncRNA does not behave exactly the same as RNA. While RNA “carries the genetic information copied from DNA” to proteins, lncRNA does not encode proteins. Instead, it is responsible for “gene inhibition and gene activation through a range of diverse mechanisms.”
"By genetically modifying a long noncoding RNA, we prevent HIV recurrence in T cells (immune cells) upon cessation of antiretroviral treatment, suggesting that we have a potential therapeutic target to eradicate HIV and AIDS,” lead author Tariq Rana is quoted as saying by The Sun.
"Our results suggest that HEAL plays a critical role in HIV pathogenesis. Further studies are needed to explain the mechanism that leads to HEAL expression after an individual is infected by HIV, but this finding could be exploited as a therapeutic target,” Rana added.
Rana did not immediately respond to Sputnik’s request for comment.