Researchers at Carnegie Mellon University now have a clue to why HIV enters immune cells so easily. Their findings could lead to new drug discoveries and possibly to preventing deadly infections.
According to Stephanie Tristram-Nagle, associate research professor of biological physics at Carnegie Mellon, HIV needs to cause the fusion between its membrane and an immune cell membrane to infect it.
Normally, a cell membrane resists curving. But in a recent study, Tristram-Nagle found something surprising. Once HIV docks onto the host immune T-cell, the HIV fusion peptide's role may be to cause the T-cell's membrane to bend more easily.
"We found that HIV fusion peptide, which is part of the larger HIV fusion protein, dramatically decreases the amount of energy needed to bend a cell-like membrane," said Tristram-Nagle. "This helps the membranes to curve and form a pore, a necessary step for HIV to fuse with an immune cell and deliver its RNA as it infects it."
Tristram-Nagle said the curving helps to explain in part how HIV infection occurs so readily.
"Our findings definitely will change how theoreticians think about virus-cell interactions," she said. "This same phenomenon could provide a general way that viruses use to infect cells, since many viruses have fusion peptides, so it will be exciting to look at other viral systems with our experimental method."
The research was conducted in collaboration with John Nagle, Carnegie Mellon professor of physics and biological sciences, and data were collected at Cornell University's CHESS synchrotron, which provides a high-intensity source of X-rays for various studies. The work was supported by the National Institute of General Medicine.