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Immune Molecule Protects Cells Threatened by HIV

Closing in on drugs that could boost the immune systems of HIV sufferers
T cell



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Researchers report that a molecule produced by the immune system prolongs the life of immune cells that would normally self-destruct as a result of HIV infection. The finding adds weight to the case for clinical trials to study whether the molecule interleukin-7 (IL-7) when combined with antiretroviral drugs can beef up the immune systems of HIV sufferers.

"It's not just the drugs that battle HIV," says researcher Paolo Lusso, a virologist and immunologist at the National Institute of Allergy and Infectious Disease (NIAID). "It's a sort of alliance between drugs and the immune system. You have to have both."

Lusso, together with leading HIV researcher and NIAID chief Anthony Fauci and their colleagues, added IL-7 to T cells extracted from people at different stages of HIV infection. Along with the T cells it infects, HIV also kills many healthy T cells—and one likely method of cell death is a spontaneous process of self-destruction called apoptosis. The team found that IL-7 warded off apoptosis in CD4+ T cells, the coordinators of the immune response, and CD8+ T cells, the immune system's roving attackers.

Although at least two clinical trials of IL-7 for HIV are in the planning stages, the evidence for its benefits had been somewhat mixed, says Lusso, whose team's study appeared online February 5 in the Proceedings of the National Academy of Sciences USA.

Lusso says the goal of treatment with IL-7 (or a related molecule in clinical testing called IL-2) is to restore some of the defense against disease that HIV erodes by keeping more healthy immune cells alive. Up to 20 percent of people with HIV who respond to antiretrovirals nonetheless fail to grow more T cells, says immunologist Alan Landay of Rush University Medical Center in Chicago. The new results strengthen the clinical case for blocking apoptosis, he says.

The researchers observed that IL-7 was more protective of T cells the more advanced the case of HIV was, Lusso says, suggesting that treatment could be more beneficial for those with advanced infections. But he adds that he is planning to evaluate IL-7's effects in monkeys shortly after they have been infected, because HIV seems to cause most of its damage early in infection.

Lusso says even a successful IL-7 or IL-2 treatment would not eliminate the virus from a person's body. For that, he says, new drugs called entry- and integration- inhibitors may be necessary. "The final [drug] cocktail," he says, "is still to be conceived."

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