Unlike a similar discovery announced last month, the new work involves strains of the virus, commonly spread from person to person.
Altogether, the discoveries are important because they are "telling us very basic things about what HIV needs to infect cells", said Dr James Hoxie, a researcher at the University of Pennsylvania who was not involved with the reported studies. "This is the first real hard insight into a process that's been very elusive until now."
Scientists have long known that to get inside cells, HIV attaches itself to a structure on the cell surface called CD4. But it has also been clear that HIV needed another foothold as well.
Last month, researchers reported that for some strains of HIV, this second foothold is a cell protein called fusin.
But fusin does not appear to be used by HIV strains that are most commonly transmitted between people and which predominate early in the course of a person's infection.
Now, five teams of scientists say they have identified a foothold for these strains.
It is a protein found on blood cells, and it normally acts as a docking site for chemokines. Chemokines are chemical messages that summon blood cells to the sites of inflammation.
Chemokines made headlines last year when research showed they could virtually stop HIV from reproducing in the test-tube.
The new work shows that chemokines keep HIV from even entering blood cells, a necessary step for HIV reproduction.
"They pretty much shut the door on the virus getting in," said one of the researchers, Dr Dan Littman, of the Howard Hughes Medical Institute at the New York University Medical Center.
Chemokines may shut the door by blocking HIV's access to their docking sites, called receptors, researchers said. So designing drugs to do the same thing may provide a new route of therapy.
The chemokine receptor implicated by the five scientific teams is called CC-CKR-5.
The research appears in the latest issue of the journal Nature and the 28 June editions of the journals Science and Cell.Reuse content