U. Medical Center researchers discover compound that slows HIV advancement

University Medical Center researchers have recently identified a molecular compound which could prevent a benign HIV infection from transforming into the lethal AIDS disease, potentially allowing HIV-positive patients to live out their natural lives. Between 650,000 and 900,000 people in the United States are HIV-positive but relatively free of symptoms. However the virus eventually leads to AIDS, which killed more than 56,000 Americans last year. In its earliest stages, the HIV virus binds to a group of "receptor" molecules found on the surface of certain cells in the body. But as it progresses, the virus binds to the type of receptor commonly associated with AIDS, according to Biomedical doctorate student Benjamin Doranz, the lead author of a report on the research. The report appeared in Monday's Journal of Experimental Medicine. This receptor, known as CXCR4, becomes the virus's entrance way into T-cells responsible for the body's ability to fight infection, hastening the onset of full-blown AIDS. Pathology Professor Robert Doms, who co-authored the report, added that "these [aggressive HIV viruses] are bad players." The report opens the door for scientists to develop a method for preventing the HIV viruses from binding to CXCR4, keeping an HIV infection from turning into AIDS. "It's thought that by blocking those specific types of virus, we might be able to slow down [HIV] infection," Doranz said. In the experiment, Doranz exposed live human cells to a mutated form of the HIV virus, which gives off light after successfully infecting a cell. He then placed a bioengineered compound into the cell culture and measured the amount of light given off by the viruses. The T-cell cultures exposed to the compound gave off the least amount of light, suggesting that those cells were not infected with HIV. These results are consistent with findings by researchers in Japan and Belgium, who published similar reports on the receptor in the same issue of the journal. Blocking all of the HIV receptors would theoretically render the virus powerless to infect any human cells and cause AIDS. "The virus can't do without [the receptors]," Doms said, adding that a compound will be found to block another receptor in the near future. "You might be able to stop the virus dead in its tracks," he said. But blocking HIV's many receptors might force it to evolve into an even more powerful virus, making it difficult to control. "You don't want to let it evolve into something worse," warned Doranz, who stressed that clinical trials will have to proceed cautiously. And the compound "is going to have to go through extensive testing in animals for toxicity," added virology expert Edward Berger, a researcher at the National Institute for Health who discovered that CXCR4 was a receptor for the HIV virus last year. "If you block [CXCR4], you might be blocking some other important function in the body," he explained. But he stressed that the Penn finding was significant and could potentially lead to new HIV therapies. "It's very important," said Berger. "It's a demonstration that, at least, in a test tube, you can get an anti-HIV effect with a small molecule that blocks a co-receptor."