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CRISPR-Cas9 gene editing could one day ‘turn off’ HIV virus in the body

HIV treatment has come a long way over the years, due in large part to antiretroviral drugs that stop the HIV virus from replicating in the body. This gives the immune system a chance to repair itself and stop further damage. Thanks to these amazing advances, HIV is no longer the death sentence that it was in previous decades.

However, antiretrovirals only keep HIV at bay for as long as they’re taken. Defaulting on the drugs means that the HIV virus comes back. Even worse, it can cause patients to build up resistance to the antiretrovirals so that they do not work so effectively in the future.

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In other words, there’s still room for improvement when it comes to treatment. Fortunately, researchers from the University of California — San Diego School of Medicine are poised to provide help, courtesy of a new genetic-sequencing approach that could possibly provide a “kill switch” to clear out dormant HIV reservoirs inside cells.

“The most exciting part of this discovery has not been seen before,” Tariq Rana, professor of pediatrics and genetics at UC San Diego School of Medicine, said in a statement. “By genetically modifying a long non-coding RNA, we prevent HIV recurrence in T cells and microglia upon cessation of antiretroviral treatment, suggesting that we have a potential therapeutic target to eradicate HIV and AIDS.”

The work is based on the discovery of a recently emerged gene that appears to regulate HIV replication in immune cells, including macrophages, microglia, and T cells. The team refers to this as HIV-1 Enchanced LncRNA (HEAL), and it is elevated in people with HIV. By using CRISPR-Cas9 gene editing, their work suggests that it could stop HIV from recurring in the event that antiretroviral treatment is stopped.

“This has the potential for [being a] cure but, [we’ll] have to wait for animal studies,” Rana told Digital Trends. As for the next steps, Rana said that future studies “will determine if turning this regulator HEAL off can remove viral reservoirs, which are the key source for viral rebound when therapies are discontinued.”

A paper describing the work was recently published in the journal mBio.

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