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AIDS Study May Yield Permanent Cure


1/3/05 - 5:00p EST

Approved in 1995, the new cocktail of drugs, individually called protease inhibitors, made a dramatic difference to the lives of the HIV positive. Within one to three months of beginning treatment with the new regimen, which has come to be known as HAART or highly active antiretroviral therapy, the 'viral load' or the measure of new AIDS viruses produced in the body, dropped to undetectable levels. Researchers were hopeful that this meant that they had found the cure for AIDS. They were wrong.

No matter how the drugs were prescribed, the virus always came back once treatment was halted. Even worse, in many cases, the virus rebounded to new high levels and was resistant to treatment if any part of the drug regimen was discontinued. It was discovered that the AIDS virus, like several other viruses such as the Herpes family, 'goes into hiding, dormant and practically undetectable in the body - and impervious to attack'.

Enter the virologists at Thomas Jefferson University's Center for Human Virology and Biodefense, led by its director, Dr. Pomerantz. Dr. Pomerantz team undertook the difficult challenge of determining if and how the latent reservoirs of the AIDS virus could be brought out of hiding and subjected to attack by the existing HAART therapy. Using samples from infected patients who had been taking the HAART cocktail and had undetectable levels of HIV in their bloodstream, the Jefferson researchers screened the cells with several different substances to determine which best caused the dormant viruses to expose themselves.

The team proved that an immune protein called interleukin-7 (IL-7) in combination with a few others, such as IL-2 and/or OKT3 can stimulate the virus better than previously tried drugs and make it vulnerable to both HAART and the bodies own immune system. If a therapy can be developed based on this finding, it may lead to a complete cure for AIDS.

Said Dr. Pomerantz, 'IL-7 may teach us something...We're not sure why only these certain strains are affected. We think we've found a new population, a new reservoir of HIV that has not been seen before. It's probably a sub-population of blood cells, lymphocytes not stimulated by IL-2 or OKT3. There could be other reservoirs as well...We may need more than one drug to stimulate virus from latency, similar to using HAART to stop replication...we may have to combine IL-2 with IL-7 and other agents to get to the reservoirs of virus.'

Steven Leser, sleser001@yahoo.com



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