AEGiS-UPI: Friendly virus may slow HIV infection United Press InternationalImportant note: Information in this article was accurate in 2001. The state of the art may have changed since the publication date.
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Friendly virus may slow HIV infection

United Press International - Wednesday, 5 September 2001
Charles Choi


IOWA CITY, Iowa, Sept. 5 (UPI) -- An apparently harmless virus known as GBV-C appears capable of improving the survival rate of AIDS patients by slowing down the growth of human immunodeficiency virus, which causes the deadly disease.

"We are now working to understand precisely how GBV-C inhibits HIV from growing," senior researcher Jack Stapleton of the University of Iowa in Iowa City, said in a statement. "Eventually, these findings may help to develop a new approach to HIV therapy, either by using the virus itself or by using GBV-C proteins to activate other proteins or immune responses that could inhibit HIV."

The medical scientists do not recommend, however, that AIDS patients run out and get infected with GBV-C.

"Absolutely not. That would potentially be very hazardous," research team member Daniel Diekema told United Press International in an interview. "It would be premature to suggest that people with HIV should be infected with GBV-C right now. Just because we think that GBV-C has no known disease association right now doesn't mean that we won't find something in the future." The virus GBV-C was once believed to cause hepatitis or inflammation of the liver. A relative of the hepatitis C virus -- which does cause liver damage -- GB virus C was first isolated in 1995 from a blood sample obtained in the 1960s from a surgeon with hepatitis. The virus draws the "GB" in its name from the initials of the surgeon.

About one out of 50 healthy blood donors in the United States is infected with GBV-C.

"Although GBV-C is very common in humans, it does not appear to cause any disease," Stapleton said in a statement. "Once it was learned that it did not actually cause hepatitis, many researchers stopped studying it. We continued to study it because we thought it might serve as a model to understand hepatitis C virus."

Four previous clinical studies already have noted a relationship between GBV-C and HIV in patients with both infections. "However, our University of Iowa studies involved 50 percent more GBV-C and HIV co-infected patients than the previous studies combined," Stapleton wrote. "In addition, our laboratory studies are the first to demonstrate an inhibitory effect of GB virus C on HIV."

The clinical part of the research team's study looked at blood samples and mortality data from 362 HIV patients who visited the University of Iowa HIV/AIDS clinic from 1988 to 2000. Nearly 40 percent of these patients also were infected with GBV-C, an infection rate similar to that in all HIV patients.

"We found that HIV-infected people without GBV-C infection were 3.68 times more likely to die than those with GBV-C," Stapleton noted. "This makes us think that GBV-C is one factor in why some people live longer and more healthily with their HIV infection than other HIV-infected people do." The laboratory portion of the researchers' study examined human white blood cells known as helper T-cells grown on lab dishes. The scientists found cells infected with both viruses produced 30 percent to 40 percent less HIV than those infected with HIV alone.

However, the researchers do not yet know why and how GBV-C slows HIV growth.

"It does not appear to prevent HIV from entering the cell," Diekema told UPI. "It probably starts working after HIV infection. It could be that GBV-C stimulates an immune response that inhibits HIV infection. It could also be that it more directly inhibits some key process of HIV replication, targeting a viral protein or something like that." One of the scientists' main concern is that there is a hidden factor that is actually responsible for the anti-HIV effect.

"The more measurements we get, the more we will have a better understanding of the science behind the mechanism, to understand whether this is a true association or not," Diekema said. "I don't see any immediate clinical applications. I do see the possibility of new treatments once the mechanism is determined."

The study is published in the Sept. 6 issue of the New England Journal of Medicine, which also contains an editorial from researchers at Northwestern University in Evanston, Ill., who stressed that while the research had "intriguing implications," there are many questions that remain to be answered and many elements of the story that remain to be discovered.

"GBV-C was only recently discovered and the potential long-term consequences of persistent infection, especially in persons with weakened immune systems, will not be known for some time," Valentina Stosor and Steven Wolinsky wrote in the editorial.

In an interview with UPI, Wolinsky added intentional inoculations with blood from GBV-C infected patients was extremely inadvisable. "GBV-C is an accidental tourist of sorts, and frequently co-exists with things such as hepatitis C and other more noxious pathogens, which makes the idea of inoculations inherently very dangerous," he said


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