That figure was about 5 percent higher than in 1999, though considerably lower than the 4,226 infections reported in 1994.

The CDC said more data was needed before researchers could conclude that AIDS was poised for a comeback among intravenous drug users, one of the groups at highest risk for the disease.

People who inject drugs and their sex partners represent about one-third of all those who have been infected with HIV in the United States since the virus first surfaced in 1981.

Tanya Sharpe, a behavioral scientist and an AIDS expert with the CDC, said the increase in diagnoses could have resulted from expanded AIDS testing or a change in risk behavior among intravenous drug users.

"It could be that some of the prevention messages have lost their fervor in the communities and the advances in anti-retroviral drug treatment may have lulled some people into a false sense of security," Sharpe said.

She said routine AIDS testing and drug treatment and counseling were the keys to controlling the epidemic among intravenous drug users.

Making AIDS tests more common is at the heart of the CDC's strategy to increase the proportion of HIV-infected persons who are aware that they carry the virus from 70 percent to 95 percent by 2005.

As many as 30 percent of the estimated 850,000 to 950,000 people living with the virus in the United States do not know that they are infected. About 16,000 Americans die each year from AIDS and another 40,000 become infected with HIV.

PARIS (AFP) - Scientists in the United States believe the AIDS virus craftily hijacks an immune cell to help it evade elimination by powerful anti-retroviral drugs.

Dismaying evidence started to emerge a few years ago that highly active anti-retroviral therapy (HAART), introduced in 1995, was not the HIV slayer that it initially appeared to be.

It was discovered that HAART can beat the human immunodeficiency virus (HIV) back to below detectable levels in the bloodsteam -- but, as soon as the medication is stopped, the virus bounces back from some hidden "reservoir," presumed to be the lymph glands.

So a frantic search was launched to find out how the virus did this disappearing trick. Until now, it has thrown up few clues.

Reporting in Thursday's issue of the British weekly journal Nature, a team led by Mario Stevenson of the University of Massachusetts Medical School says that HIV-1 uses a "pirate protein" to hide inside inactive immune cells, then reappears at a later date.

The virus first infects a cell called a macrophage, inducing it into producing a viral protein called Nef.

Nef then prompts the macrophage into releasing a couple of other proteins called soluble factors, which go on to stimulate other components of the immune system that are called B cells.

These subverted B cells then come into contact with inactive defenders of the immune system -- resting T cells -- and in effect open up the T cells, making them vulnerable to infection by HIV.

It amounts to an astonishingly complex ballet by signalling molecules.

In particular, it smashes a hole in the prevailing belief that HIV-1 could infect only T cells that had been activated after encountering an invader and were starting to replicate.

"Nef seems to engage in molecular piracy, taking over an existing cellular pathway and allowing HIV-1 to replicate in T cells in diverse activation states," said Roger Pomerantz, of Thomas Jefferson University, Philadelphia, in an commentary published in Nature.

The data show "there is an entire spectrum of interactions between the virus and host cells, which together produce the general pattern of HIV-1 reservoirs and residual disease."

HIV-1 is by far the dominant strain of the two strains of HIV virus that have been discovered in the 22-year AIDS epidemic.

More than 60 million people have been infected by the virus, over a third of whom have died.