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Harmless virus helps slow HIV by boosting immune proteins

ll expressed and secreted"). This protein naturally occupies the same molecular docking site favored by HIV-a receptor called CCR5-and thus keeps the AIDS virus from binding to white blood cells and gaining a foothold in the body.

Drugs are under development that mimic the effect of these chemokines. However, Stapleton believes GBV-C itself should be seen as a potential HIV treatment because of its safety profile and because patients would need only a limited number of exposures to see benefits. He and his colleagues are now considering a clinical trial in which HIV patients would be infected with the virus.

"The fact that GBV-C is such a common infection, and that's it's been so extensively studied and not shown to cause any diseases, distinguishes it from other live viruses and makes it a more realistic option," said Stapleton. He pointed out that the Food and Drug Administration does not require blood donations to be screened for GBV-C, even though about 1 in 70 units of blood in the United States contains the virus.

Currently there is only one medication available, Fuzeon, that blocks HIV at the early stage of the virus' replication, before it even enters T cells. But this drug costs up to $25,000 per year and must be given by injection twice daily. Other drugs that work similarly are under development.

While many HIV patients today are helped by highly active antiretroviral therapy, or HAART, many become resistant to the drugs. Stapleton said the effect of GBV-C on HIV viral load is similar to that of HAART, though not as potent. The likelihood of resistance, however, is much lower with GBV-C.

"HIV probably doesn't become resistant to GBV-C very easily, but it is possible to lose the virus," said Stapleton. "We have to figure out how this can be prevented."

Collaborating with Stapleton and Xiang on the study were Drs. Sarah George and Sabina Wunschmann, along with Qing Chang and Donna Klinzman. The work, pre
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17-Jun-2004


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