Researchers at the University of California, San Diego and Oak Ridge National Laboratory have discovered how a genetic circuit in HIV controls whether the virus turns on or stays dormant, and have succeeded in forcing the virus towards dormancy. Further studies are under way on the feasibility of using this approach for anti-HIV therapy.
The scientists explored the Tat circuit - the genetic master circuit of HIV - and built upon previous work that showed that it did not function like a standard on-off switch. The HIV circuit is driven by cellular noise, or random events, which activate the circuit for a limited amount of time before it turns off.
In the current study, the scientists were able to exploit this noise in the HIV Tat circuit to measure how long HIV remained activated in the cell, and deduce that the time spent in the active state drove HIV's
decision to destroy the cell or not. Then the researchers increased the levels of the native cellular gene SirT1 - a gene implicated in aging - to reduce the lifespan of the HIV virus and force HIV-infected cells to
go dormant.
