Scientists Unravel New Clues About HIV

LONDON (Reuters) - Scientists have identified a protein that permits HIV, the virus that cause AIDS, to evade the immune system.

The protein, called Nef, protects HIV-infected cells and at the same time destroys other healthy cells in the immune system, assuring that the virus will thrive.

``This reveals a real, unfortunate, elegance to HIV in terms of its ability to kill off cells that are trying to control the virus, and at the same time to defeat that same cell-death machinery in the host cell thereby allowing the virus to replicate, all through the same regulatory protein,'' said Warner Greene, of the Gladstone Institute of Virology and Immunology.

``It is a remarkably efficient and cunning strategy.''

Scientists have known that healthy cells around the infected HIV cell self-destruct and that Nef played a role, but until now they didn't know how.

Greene and his colleagues have shown that Nef binds to and inhibits a protein called ASK1 which is a key to the destruction of the healthy cells.

Their research, reported in the science journal Nature, could provide a new target for drugs to combat AIDS, which has killed nearly 22 million people since the start of the epidemic two decades ago.

``If we could effectively block the assembly of Nef and ASK1, it could lead to the premature death of the HIV-infected host cells,'' Green added.

``The HIV infection process would then be short-circuited and the virus might simply die out because it would not have sufficient time to fully reproduce itself.'' CASES OF DRUG RESISTANT HIV ON THE RISE

If researchers could find a molecule to block the interaction of Nef and ASK1, it would open up a new line of attack against the virus.

``I think more and more attention is going to focus on the regulatory proteins of HIV as drug targets,'' Greene added.

The three classes of drugs currently used to battle the human immunodeficiency virus work by interrupting its life-cycle.

Nucleoside Reverse Transcriptase Inhibitors (NRTIs) mimic one of the building blocks of DNA and interfere with the enzyme needed for retroviral replication.

Protease Inhibitors (PIs) block another viral enzyme, protease, needed by HIV to make new copies of itself. Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs) block reverse transcriptase directly.

The drug combinations have prolonged the lives of HIV sufferers, but the virus' cunning ability to mutate makes drug resistance an increasing problem.

By concentrating on Nef, Greene and his team are aiming at cell proteins that HIV needs to grow and spread.

The researchers have also been encouraged by the fact that people with HIV strains lacking the Nef gene develop symptoms of the disease much more slowly than other people.

``If we can win the battle at the single cell level, then we will be in a better position to win the war in the millions of HIV infected patients,'' said Greene.

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