A protein, called CAML (calcium-modulating cyclophilin ligand) prevents the release of HIV-1 virus from human cells and could now be a target for new HIV treatments, scientists have revealed.
It's long been known that a majority of human cells carry a factor that controls the discharge of virus particles. However, it is now that the research team rom Emory University School of Medicine, Vanderbilt University School of Medicine, and Mayo Medical School has identified CAML as the cellular protein that inhibits the release of HIV particles.
Usually, CAML hinders a very late step in the virus lifecycle, which results in the retention of HIV particles on the membrane of the cell. The virus has an inbuilt mechanism to cancel out CAML, by the action of the viral Vpu protein.
In the absence of Vpu, HIV particles are not cut off from the plasma membrane, but accumulate by a protein bound at the cell surface.
After depleting CAML in human cells in the laboratory, the researchers found that Vpu was not needed anymore for felicitating smooth exit of HIV-1 particles from the cell. After expressing
When they expressed CAML in cell types usually permitting particles to exit freely, they found that the particles remained attached to the cell surface.
"This research is important because it identifies CAML as an innate defense mechanism against HIV. We are continuing to work on the mechanism that Vpu uses to counteract CAML and on defining exactly how CAML leads to virus particle retention on the infected cell membrane. We hope this will lead us to new treatments," Nature quoted senior author Paul Spearman, professor of pediatrics (infectious diseases) at Emory University School of Medicine, as saying.
The research is published in the advance online edition of Nature Medicine.