This understanding of how the virus deactivates the immune cells could lead to methods in overcoming the prevailing handicaps in treating HIV, the scientists feel.

    As HIV accumulates in the blood, specific immune cells that target viruses called CD8 begin to over-produce a receptor molecule called Programmed Death-1. As this PD-1 builds up on the surface of the CD8 cells, the immune cells became weaker and produced fewer virus-killing chemicals, such as cytokines.

    Instead of functioning as sentinels of the immune system, the CD8 cells gradually burn out, becoming clogged-up with PD-1. The immune cells are there, but they have been turned off in persons with high viral loads, says Bruce Walker at Massachusetts General Hospital in Boston, US, who led the research.

    He said: "But it did not make sense that these cells were found in high numbers in persons with late stage AIDS, indicating they were somehow not doing their job."

    "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."

    Rowland-Jones, who wrote a commentary piece accompanying the study in Nature, warns that blocking PD-1 altogether could be dangerous. She says that in experiments on mice bred to lack the gene, the mice developed severe autoimmune disease.
This suggests that the protein plays an important role in stopping the immune system attacking itself. Perhaps, she says, HIV exploits this to blind the immune system to its presence.

    Researcher Dr Cheryl Day, of the University of KwaZulu-Natal, Durban, added: "Natural regulatory systems that help control the immune system appear to be shutting it down before its work is done.

    "One of the next questions we need to answer is whether we can turn it back on for HIV-infected patients in a way that will benefit them without incurring serious side effects."Enditem

(Agencies)