HIV "disables" immune cells

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Scientists believe they have determined how T cells - central cells in the immune system - in patients with HIV are "disabled", weakening the body's natural defence mechanisms against different viruses.

Researchers from a number of institutions, including the Partners Aids Research Centre (Parc) at Massachusetts general hospital (MGH), set out to determine why the immune system is unable to control HIV infection.

Earlier studies found that blocking a protein known as PD-1 in infected mice could help to boost ailing T cells to fight infection.

In the most recent study, published in the journal Nature, the researchers found that chronically-infected HIV patients have dramatically more PD-1 receptors in their cells, suggesting that CD8 cells, which should destroy virus infected cells, "were somehow not doing their job".

Commenting on the results of the latest study, Dr Bruce Walker, lead author of the study, said: "These new findings finally make sense out of our early discoveries and subsequent findings by others in the field: the immune cells are there, but they have been turned off in persons with high viral loads."

Laboratory tests found that antivirals blocked this 'molecular switch', decreasing PD-1 levels and increasing CD 8 cells ability to respond to viruses.

"It has been thought that the ineffectiveness of HIV-specific T cells resulted from progressive, irreversible damage or bad cellular 'programming'," said Parc's Dr Daniel Kaufmann, a co-author of the paper.

"While this might still be partially the case, our finding that defects in important functions of exhausted T cells can be reversed demonstrates that active inhibitory mechanisms may play a major role in blocking T cell function. In other words, the cells may be turned off but not permanently disabled."

The scientists concluded that the next step is to establish whether the effect on the immune system in HIV-infected patients could be reversed "in a way which will benefit them without incurring serious side effects".


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