"The more of these [messages] sensed within the cell, the more Tat proteins the gene creates, resulting in a snowball effect that is difficult to stop," Weinberger said of the onset of full-blown infection.
Mechanisms do exist to halt the process, however. For example, another enzyme within the affected cell called SirT1 is capable of pulling the chemical tail off the Tat protein, rendering it silent. The interplay between p300 and SirT1 comprises the resistor and can effectively keep the virus in its dormant phase.
"SirT1 reduces the strength of the signal to replicate," Weinberger said. "It may prove to be the key part of the resistor in the circuit, as our mathematical models are strongly suggesting."
Not all the molecular players are known yet, nor how their relative roles determine whether the virus becomes dormant, but Weinberger said his and Shenk's results lead them to think they are on the right track. If their theories prove correct, they could form the basis for therapies that combat HIV and other viruses that possess these genetic circuits within their own DNA.
"SirT1 and related processes might eventually turn off viral activation in T cells all by themselves, but the cell is usually dead before it can happen," Weinberger said. "If we can create drugs that target these enzymes, perhaps we can get SirT1 and related enzymes to assert themselves immediately, forcing HIV into h