Protective virus ties up HIV docking sites

In 2001, two groups of scientists reported that people with HIV are much less likely to die from AIDS if they’re concurrently infected with a harmless virus called GBV-C (SN: 10/6/01, p. 216: For a change, infection stymies HIV). One of the research groups has now uncovered a mechanism by which this protection might be conferred.

GBV-C, originally misnamed hepatitis G, occupies molecular receptors on the surface of CD4 T cells, the immune cells typically hijacked by HIV, the scientists report. These receptor molecules, called CCR5 and CXCR4, are also ports for HIV. Tests in laboratory dishes show that once occupied by the GBV-C virus, the receptors can’t take on the more dangerous HIV.

“GBV-C decreases the number of [available] receptors on the surface of a cell, and that limits the amount of HIV getting into cells,” says Jack T. Stapleton of the University of Iowa in Iowa City. This binding thwarts HIV from replicating within and killing these immune cells.

The test-tube findings might explain why coinfection with GBV-C inhibits HIV from disabling the immune system in HIV-positive people, Stapleton suggests. He presented the findings at the 10th Conference on Retroviruses and Opportunistic Infections in Boston last month.


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