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Scientists have known for a long time that the HIV virus, upon entering a cell, can lie dormant for some time before becoming active.
Researchers from Princeton University are trying to understand the biology behind this On/Off switch for HIV and how to exploit it for use in developing anti-HIV treatments.
In an article published in the journal PLoS Biology the researchers, Leor Weinberger and Thomas Shenk, explain that the HIV virus becomes dormant by turning off its genes and shutting of protein synthesis.
The Tat protein (encoded by the HIV Tat gene) was a likely target for this molecular switch because it was known to regulate its own gene expression as well as the expression of other genes.
They used a mathematical model to predict how this protein could be switched on and off during HIV's latent stage and went on to confirm the model in a cell culture system.
They found that the SirT1 protein acts as an inhibitor of Tat and functions as part of a "feedback resistor" pathway in which Tat's off position overpowers the on position during HIV latency and most other circumstances.
However, the off position is unstable. Tat can turn itself on in response to random increases in its activity or in response to environmental inhibitors of SirT1 such as dihydrocoumarin, a natural flavoring agent found in clover.
While it is exciting that researchers have identified components of this on/off switch system, more research must be done to find ways to affect and manipulate it. If researchers can find a way to keep the switch in the off position they can exploit this knowledge to develop new anti-HIV drugs.
