Press Release

Infection with 'friendly' virus may help HIV patients

VA R&D COMMUNICATIONS/AUG. 22, 2001

You would think the last thing people with HIV need is to be infected with another virus. But an Iowa City scientist has found that a form of hepatitis virus called GBV-C may actually prolong the life of patients with HIV. The "friendly" virus works by keeping the deadly AIDS virus from replicating.

Reporting on his team's study in the September 6 New England Journal of Medicine, Jack Stapleton, M.D., of the Iowa City Veterans Affairs (VA) Medical Center and the University of Iowa says GBV-C itself appears to cause no symptoms and therefore may one day pose a new therapy for HIV. About 1 million Americans are infected with HIV, and more than 2.5 million deaths are related to HIV each year worldwide.

In a study of 362 patients with HIV, Dr. Stapleton and colleagues found a lower death rate among those who also had the GBV-C infection-28.5 percent compared to 56.4 percent. Of 218 HIV patients without the hepatitis virus, 123 died during the 12-year study period. Of 144 patients co-infected with GBV-C, 41 died.

The new study confirms the results of earlier, smaller studies on the connection between GBV-C and HIV, and adds a new twist: The VA team showed that infecting human blood cells in the laboratory with GBV-C slows the rate at which the AIDS virus multiplies.

According to Dr. Stapleton, a virologist and infectious disease specialist, outside of experimental gene therapy there are few if any examples of treating an active disease with a virus. But he said viruses, like bacteria, can at times be beneficial.

"People don't think about the 'friendly neighborhood virus.' Yet undoubtedly this happens," said Dr. Stapleton. "The human genome is full of retrovirus sequences. The harmful ones have no doubt been largely deleted by natural selection, and the ambivalent or beneficial ones stick around."

About 15 percent of people with Hepatitis C, a common form of liver disease, are also infected with GBV-C, originally known as the Hepatitis G virus. Among people with HIV, the figure rises to at least 30 percent. But unlike the Hepatitis C virus, GBV-C does not appear to cause any symptoms.

"We would not predict any side effects to be associated with GBV-C as a treatment. It has not been associated with any clinical illness," said Dr. Stapleton, adding that the Food and Drug Administration and blood-banking authorities do not require screening blood donors for the GBV-C, even though it is estimated that at least 1 of every 100 donors has the virus and may transmit it.

Dr. Stapleton and his team plan further research to pinpoint the effect of GBV-C on HIV. They believe the virus may induce certain cellular responses, such as increased production of interferon or other cytokines, that hamper HIV replication.

Collaborating with Dr. Stapleton on the study were Jinhua Xiang, Sabina Wunschmann, Daniel J. Diekema, Donna Klinzman, Kevin D. Patrick and Sarah L. George, all with the Iowa City VA Medical Center and the University of Iowa College of Medicine. Dr. Stapleton is a VA researcher and staff physician, and director of the Helen C. Levitt Center for Viral Pathogenesis and Disease at the University of Iowa. The research was supported by VA and the National Institutes of Health.

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