GBV-C is related to the virus that causes hepatitis C. However, it does not infect liver cells, and causes no form of hepatitis. Rather, like HIV, it infects white blood cells-specifically, helper T cells. It is also contracted in the same way as HIV-through bodily fluids. About 10 to 15 percent of healthy blood donors either have active GBV-C infection or antibodies indicating past exposure. Almost 90 percent of people with HIV, according to some studies, show evidence of having been infected with GBV-C, but about half of these patients develop antibodies that knock the virus out of their system.

GBV-C was first identified by scientists in 1995, though studies suggest it has been around since ancient times. The idea that GBV-C may delay HIV disease progression and lower mortality has been debated among AIDS scientists because of mixed research findings. Ten studies, by eight different groups of researchers, including Stapleton's, have shown improved survival or other clinical benefits among HIV patients who also have GBV-C. A few studies, though, showed no benefit.

The March 2004 study in the New England Journal of Medicine, co-authored by Stapleton and led by Carolyn Williams, PhD of the National Institute of Allergy and Infectious Diseases, was the most comprehensive GBV-C study to date. According to Stapleton, it showed that the duration of GBV-C infection may be critical in increasing survival, and this may help explain why other studies failed to find any effect.

"The survival advantage of GBV-C appears to depend on how long the GBV-C infection persists," said Stapleton, a staff physician at the Iowa City VA Medical Center and professor of medicine at UI.

According to the new findings by Stapleton and Xiang's team, GBV-C raises the blood levels of several chemokines, including one called RANTES (an acronym for "regulated on activation, normal T ce
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17-Jun-2004