If the battle against HIV, the virus that causes AIDS, is a chess match, then new research published today gives new insight into one of the virus' most important moves.
The findings, by University of Tennessee, Knoxville, and Oak Ridge National Laboratory researchers Michael Simpson and Roy Dar, with colleague Leor Weinberger who led the research at the University of California, San Diego, reveal new information about how a critical genetic switch in the virus operates. They are published as a letter in the upcoming issue of Nature Genetics.
When HIV infects an immune cell, it can enter one of two states: activation, where the virus replicates and then destroys the host cell; and latency, where the viral genetic material continues to exist in the cell, but there is no production of additional virus.
"While latency is a ticking time bomb," said Simpson, "a possible therapeutic goal could be to stably maintain latency indefinitely."
Previous work by Weinberger found that the genetic circuit that controls whether HIV chooses to go active or latent is not a simple "on-off" switch, but instead is controlled by a type of genetic pulse -- when the pulse lasts a certain amount of time, the switch will activate replication of the virus.
Now the three researchers have demonstrated that it is possible to manipulate the lengths of the pulses in a way that would favor the selection of latency.
This is vital, said Simpson, because the switch is a definitive factor in whether the virus will become active. If the pulse does not last long enough, he said, the virus cannot become active.