Though Weinberger emphasized the significance of the discovery was primarily for fundamental science research, he said that potential applications to HIV might be an improvement over drug cocktails, which are the mixtures of antiviral agents that have been the best-available treatment for the disease for a decade.
"Drug cocktails extend the life of the patient, but they do not completely alleviate the symptoms of HIV, nor do they work for all victims," Weinberger said. "Even when the cocktails get most of the infectious virus in a victim's body, some viruses will escape because they have hidden by going dormant. Eventually, these dormant viruses wake up and the infection returns, so it makes sense to try to keep the virus asleep if possible."
HIV weakens the body's immune system by invading CD4+ T cells, which in essence serve as the metaphorical generals in the body's defense system against illness. When an HIV virus particle invades a T cell, most often it converts the cell into a factory for making other viral particles, killing the cell in the process. Without these T cells, the body loses its ability to repel other infectious bacteria and viruses, and eventually dies from assaults from these other "opportunistic" infectious invaders.
On rare occasions, however, a virus will infect the T cell and become dormant. Why this individual viral infection would not begin to replicate when others do remains a mystery.
"It's somewhat like the unpopped kernels of corn left in the bottom of the bag when you take it out of the microwave," Weinberger said. "They were exposed to the same heat as the others but did not pop. We wanted to know why about one in a million HIV particles didn't 'pop' immediately like all the rest did."
Weinberger and Shenk found the answer in a strand of HIV's DNA where a genetic circ