An international study led by MELIS-UPF researchers has identified Schlafen 12 (SLFN 12) as a novel HIV restriction factor. The study, published in Communication Biology, reveals that SLFN 12 shuts down viral protein production, resulting in HIV-infected cells remaining invisible to the immune system and anti-HIV therapies.
Through their research, the scientists discovered a protein called SLFN12, which can limit the production of viral proteins by cleaving certain cellular tRNAs used to build proteins. The study revealed that SLFN12 can target HIV protein production precisely without affecting the production of other cellular proteins. If SLFN12’s antiviral functions are blocked, viral protein expression could increase, making it easier for the immune system and antiviral drugs to eliminate viral reservoirs. These findings offer an opportunity to develop new therapeutic approaches to combat HIV.
“Latency is a major barrier impairing virus elimination in HIV-infected individuals. We will not be able to cure an existing infection until we will get rid of latently infected cells. This is why it is essential to understand how latency works,” explains Andreas Meyerhans, ICREA research professor at UPF, who coordinated the study with Juana Díez.
The study also demonstrates how SLFN12 can specifically inhibit HIV protein production without blocking cellular protein production. The researchers explain that SLFN12 cleaves Leucine-UUA tRNA, which is rarely used for cellular proteins but essential for HIV viral proteins. These findings show that blocking SLFN12 antiviral functions should increase viral protein expression, making the virus visible to the immune system and antiviral drugs, making it easier to eliminate latently infected cells.
SLFN12 was found to specifically inhibit HIV protein production without blocking cellular protein production, helping pave the way for new therapeutic strategies against HIV, improving the quality of life of HIV-infected individuals and eliminating HIV-infected cells.