The researchers, who infected cells from Old World monkeys with HIV-1, found that cyclophilin A changed the shape of the virus particles, reports the latest issue of New Scientist.
This trick made the virus vulnerable to attack by TRIM5-alpha, part of the monkeys' innate immune system, which stops it in its tracks, but it was a different story when they infected human cells with HIV-1.
They found that the human form of cyclophilin A still changed the shape of the virus particles, but only to make them more infectious.
HIV-1 has the ability to tolerate cyclophilin A activity when it gets into human cells and the virus is using cyclophilin A to help it replicate, leading researcher Greg Towers was quoted as saying.
The changes to HIV-1 that allowed it to infect human cells might have occurred long before it actually crossed over to humans, according to Towers.
He said the researchers were a step closer to understanding how the innate immune system and HIV work together, and to discovering the interactions that allow the virus to cross the species barrier.
"The more we understand, the more likely we are going to be able to design improved therapeutics," Towers said.