Jefferson virologists coax HIV out of hiding
New technique could lead to more effective therapies for AIDS
When researchers came up with the powerful cocktail of anti-HIV drugs known as highly active antiretroviral therapy (HAART), they hoped they had found a way to finally rid the body of the virus. But they were wrong. The virus instead goes into hiding, dormant and practically undetectable in the body – and impervious to attack. While HAART manages to keep the virus at bay, its still quite capable – given the right opportunity – of replicating and wreaking havoc on the bodys immune system.
Now, virologists at Jefferson Medical College, led by Roger J. Pomerantz, M.D., professor of medicine, biochemistry and molecular pharmacology and director of the Division of Infectious Diseases and Environmental Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia, may have found a way to bring HIV out of hiding. They have shown that an immune cell protein called interleukin-7 (IL-7) can rouse the virus better than previously tried agents, making it vulnerable to drugs and the bodys immune system. If the new technique proves its mettle, the work could lead to improved treatments for HIV infection, and might be a step toward complete viral eradication.
The Jefferson team reports its findings January 4, 2005 in the Journal of Clinical Investigation.
Dr. Pomerantz, who is director of Jeffersons Center for Human Virology and Biodefense, and his co-workers took blood cells from HIV-infected patients who had been taking HAART and who had undetectable levels of virus. Using a special technique, they screened the cells with several different drugs to determine what stimulated the latent virus the best. "To our surprise, it was IL-7," he says. "We dont know why, but it is the best agent in terms of its ability to stimulate HIV out of latency that weve seen in the last 15 years." They found that the virus was stimulated to higher levels and was activated in more patients than with other compounds.
Dr. Pomerantzs group also discovered that IL-7 appears to stimulate a group of sub-strains of HIV that are different than those brought out of latency by other agents, such as IL-2, another immune cytokine, or OKT3, a monoclonal antibody. He suspects such strains may be from an unknown viral reservoir in the blood. "IL-7 may teach us something," he says. "Were not sure why only these certain strains are affected. We think weve found a new population, a new reservoir of HIV that has not been seen before. Its probably a sub-population of blood cells, lymphocytes not stimulated by IL-2 or OKT3. There could be other reservoirs as well."
Ultimately, he says, the answer to the latency problem may entail using a combination of drugs. "We may need more than one drug to stimulate virus from latency, similar to using HAART to stop replication," he says, referring to this approach . "We may have to combine IL-2 with IL-7 and other agents to get to the reservoirs of virus."
Steve Benowitz | EurekAlert!
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