Carnegie Mellon University scientists found that after HIV docks onto a host cell, the Fusion Protein (FP)-23 dramatically lowers the energy required for a cell membrane to bend, making it easier for the virus to infect immune cells. FP-23 is already suspected of playing several roles in viral fusion, according to the researchers.
“Reducing this energy should help explain in part how HIV infection occurs so readily,” says Stephanie Tristram-Nagle, Ph.D., associate research professor of biological physics. “Our findings definitely will change how theoreticians think about virus-cell interactions. This same phenomenon could provide a general way that viruses use to infect cells, so it will be exciting to look at other viral systems with our experimental method.”
The Carnegie Mellon team quantified structural properties of different lipid bilayers seeded with FP-23 peptides. They found that the fusion peptide, part of FP-23, affected the energy of the manufactured lipid bilayers, which were designed to mimic normal cell membranes. They observed that FP-23 reduces the energy required to penetrate an artificial cell membrane by up to 13-fold, depending on the thickness of that membrane.
The finding will be published in the Biophysical Journal.