The findings provide the clearest insight yet into the biological mechanisms of GBV-C, a benign cousin of the hepatitis C virus. The virus infects almost all HIV patients at some point in their illness, but seems to cause no harm by itself. When present over several years, the virus appears to slow HIV growth and keep patients from developing full-blown AIDS.
A study by the Iowa City team and other collaborators published in the March 4, 2004, New England Journal of Medicine found that 75 percent of men with persistent GBV-C infection survived at least 11 years after their HIV diagnosis, versus only 16 percent of men who were initially co-infected with GBV-C but cleared the virus over time. The men had been studied before the advent of effective HIV medications.
In the new study, the Iowa City scientists infected white blood cells with GBV-C and HIV and compared them to cells infected only with HIV. The cells with GBV-C showed an increase in certain chemokines, or immune-system proteins. These proteins bind to the same white-blood-cell receptors-molecular "docking sites"-used by HIV. When the receptors aren't available, HIV is unable to infect the cells.
When the researchers neutralized the chemokines with antibodies, GBV-C had no protective effect. HIV was free to enter host cells and proliferate.
"The next thing we have to do is determine a way to mimic the effect of this virus [GBV-C] and learn how to make it persist, so it can continue to induce these chemokines and these changes in the cell that help HIV," said senior investigator Jack Stapleton, MD of VA and UI. Lead author was Jinhua Xi