Researchers may have solved key HIV mystery
Some patients don't respond well to AIDS cocktail
MINNEAPOLIS -- University of Minnesota researchers may have unlocked another key mystery surrounding HIV, the virus that causes AIDS.
The discovery appears to explain why a quarter of the patients infected with the AIDS virus respond poorly to the powerful drug cocktails while others show dramatic improvements. It still has to be confirmed by a larger study.
If the initial findings turn out to be accurate, the discovery could be used to predict how well patients will respond to drug treatments. It also could lead to more effective therapies and potential cures for a disease that currently infects about 60 million people worldwide, said Dr. Timothy Schacker, an associate professor of medicine and author of the study.
The study will be featured in the Oct. 16 issue of the Journal of Clinical Investigation.
Although the drug cocktails are far from being a cure and are associated with serious side effects, they have had a remarkable impact on the lives of millions of HIV patients since their introduction in 1996.
Doctors measure the effectiveness of the drug therapies by the amount of virus found in the blood and by the number of CD4-T cells found in the lymph nodes. The goal is to eliminate the virus from the blood and boost the CD4-T cell count to strengthen the immune system.
CD4-T cells -- a key component of the body's immune system -- live and multiply in lymph nodes but are frequently sent out like soldiers on missions to fight off bacterial and viral invaders. But in people infected with HIV, the virus invades the lymph nodes and relentlessly attacks the CD4-T cells.
Studies show that about 25 percent of patients who have no AIDS virus in their blood following drug treatment do not experience a corresponding improvement in their CD4-T count, Schacker said.
To unlock this mystery, Schacker and his colleagues removed up to four lymph nodes from each of 11 patients over a six-month period and examined them for damage.
They found that in some patients, inflammatory cells sent in by the body to help fight the AIDS virus inadvertently caused damage to the lymph tissue. This damage, in turn, triggered the formation of scar tissue, which prevented CD4-T cells from replicating in their lymph-node homes.
Schacker said he and his colleague now want to expand the study up to about 30 patients and see if the discovery has clinical applications. "We think it has uncovered an important feature in how the virus works."