The Aids virus disables one of the human body's defensive systems which would normally disrupt its attempts to attack healthy cells, say researchers.
HIV particles attack a t-cell
It is hoped the discovery, by scientists in the US and London, could lead to fresh ways of treating HIV.
The scientists believe HIV releases a protein which counteracts the body's efforts to fight it off.
But they believe the protein has at least a couple of "weak spots" that could prove to be targets for new drugs.
The studies represent more compelling evidence of the sophistication of HIV's ability to attack the body - a quality which has made it one of the leading killers in the developing world.
The virus targets a particular type of immune system cell called the T-cell, and it is the gradual depletion of these which renders the body vulnerable to Aids-related illnesses such as TB and certain types of cancer.
Scientists have been examining for years why HIV is so efficient in its attempts to infect T-cells with little or no effective intervention by the body's defences.
There is one mechanism used by the body to target viral "particles" and disable them before they can attack other cells.
A body chemical called a protein is released, which appears to be able to incorporate itself into the viruses and change their genetic code.
However, the major strain of HIV appears to have acquired the ability to block this protein - by releasing a protein of its own which locks onto the body's version and stops it getting into the virus.
In fact, it actually uses a human cell "waste disposal" system to tag the defence protein for destruction.
This ensured that it is broken down and eliminated from the cell, leaving HIV to get on with the task of making thousands of copies of itself ready to spread infection further.
Scientists hope that new drugs can now be developed to tackle the HIV protein.
In theory at least, if this was knocked out, the human defences would stand a far better chance against HIV.
Dr Michael Malim, from Guy's King's and St Thomas' School of Medicine in London, said: "We suggest that those enzymes that impact HIV-1 replication deserve consideration as potential targets of future therapeutic strategies against HIV/Aids."
The same findings were discovered by a separate team from Oregon Health and Science University.
Researchers there wrote: "These results are encouraging from a drug development perspective."