TUESDAY, March 16, 2004 (HealthDayNews) -- Some immune cells shut down before they've finished destroying invading viruses such as HIV, and scientists have been stumped as to why.
But new research in mice suggests it may have something to do with the body's need to protect itself from the havoc caused by overheated immune cells.
The findings could lead to new medical treatments if researchers can confirm the findings and develop a way to keep the worker cells on the job. "This is one of the first studies to show that it may be possible in the future to manipulate the natural immune system to make it work better," says Dr. Douglas Nixon, an associate professor of medicine at the University of California at San Francisco.
Over the past decade, drugs known as antiretrovirals have revolutionized the treatment of viruses such as AIDS and hepatitis. When used in combination, the drugs often successfully stop the AIDS virus from replicating.
But the AIDS virus is slowly developing resistance to the drugs, and the medications don't work for everyone. Researchers continue to look for new ways to keep the virus and its counterparts at bay.
In the new study, federal researchers examined the interplay between two types of immune cells known as CD8+ T cells and CD4+ T cells. They wanted to find out why the immune system disengages itself and lets the body be chronically infected by a virus, explains study co-author Kim J. Hasenkrug, a researcher with the National Institute of Allergy and Infectious Diseases.
One theory is the immune system turns off to keep itself from losing control and attacking the body, Hasenkrug says. In autoimmune diseases such as lupus, the immune system goes haywire and assumes the body's own cells are invaders.
The suppression of the immune system is probably a "normal biological process," Hasenkrug says. "During the acute phase of infection you want to have this huge response. If you don't shut down your response as the infection goes away, you run the risk that the immune system can cause as much or more damage as the virus."
The researchers infected mice with a virus that's similar to AIDS in people and watched what happened. The findings appear in the March issue of Immunity.
The CD4+ cells, which tell the CD8+ cells whether to "kill or be quiet," eventually stopped giving orders to attack, Hasenkrug says.
But by using a disease-fighting antibody to tinker with the immune system, researchers were able to prevent the attack cells from halting their virus-killing work, Hasenkrug says.
There's still plenty of research to be done on this front, Hasenkrug adds. No one knows if the approach will work the same way in humans. "Hopefully, we can develop therapies to eliminate persistent or chronic infections."