Researchers have identified a new protein that participates in HIV’s replication process, opening the door for development of a potential therapy targeting the protein. Scientists at the Salk Institute found that a protein known as Ssu72 interacts with a HIV-generated protein known as Tat, which is integral to the virus’s life cycle, to prompt dormant HIV to begin replicating. They published their findings in Genes & Development.

Ssu72 is a phosphatase, an enzyme that binds to Tat and helps begins viral transcription, and also creates a kind of feedback loop that accelerates the process.

“Tat is like an engine for HIV replication and Ssu72 revs up the engine,” Lirong Zhang, one of the first authors of the study and a Salk researcher, said in a press release. “If we target this interaction between Ssu72 and Tat, we may be able to stop the replication of HIV.”

Previously, scientists at the institute’s Regulatory Biology Laboratory discovered the CycT1 protein, which also interacts with Tat to start the viral replication process. But CycT1 is needed for normal cell function, making it a less-than-ideal candidate for a therapeutic target. On the other hand, Ssu72 isn’t needed for developing RNA for most human cell genes in the way it is instrumental to HIV’s life cycle. So the research team is planning to investigate how they can target the protein, perhaps by inhibiting its ability to prompt viral transcription. They are also studying whether low levels of Ssu72 result in CD4 cells going into a resting state.

To read the study abstract, click here.

To read the press release, click here.

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