An international study coordinated by researchers from MELIS-UPF has identified a novel HIV restriction factor called Schlafen 12 (SLFN 12). This protein disrupts viral protein production, allowing HIV-infected cells to evade anti-HIV therapies and immune responses. SLFN 12 specifically cleaves Leucine-UUA tRNA, which is crucial for HIV protein synthesis but minimally impacts cellular proteins. This discovery could pave the way for new therapeutic strategies aimed at curing HIV infections by targeting latently infected cells. Latency poses a significant barrier to effectively eradicating HIV, as these cells remain hidden from both the immune system and antiviral treatments.
The research highlights that inhibiting SLFN 12’s antiviral function could enhance viral protein expression, rendering the latent virus visible again. This visibility would allow the immune system and antiviral drugs to effectively target and eliminate these reservoirs of latent infection. The study, published in Communication Biology, emphasizes the importance of understanding how SLFN 12 operates, as this knowledge is crucial for developing successful therapies against HIV. Overall, these findings offer hope for improved strategies to combat HIV by potentially eliminating latently infected cells and curing the infection.
