Fusion factor in AIDS cells identified.

Fusion factor in AIDS cells identified

Researchers report identifying a molecule on the surface of white blood cells that helps AIDS-infected cells fuse with--and pass their infection to -- uninfected cells. The work helps explain how the AIDS-causing virus, HIV, spreads from cell to cell in infected individuals. Clinical applications remain speculative, but researchers say the new information may prove helpful as physicians experiment with novel means of controlling AIDS progression in HIV-infected individuals.

Scientists know that HIV-infected cells can bind to and then fuse with other cells, thus allowing an exchange of viral contents. They refer to the process of cell fusion as syncytium formation. In AIDS patients, cell-cell binding is mediated in part by a viral protein, gp 120, which HIV-infected cells feature on their outer membranes. This binds to a receptor called CD4 on uninfected cells, providing cell attachment--the first step in syncytium formation.

James E.K. Hildreth and Rimas J. Orentas of Johns Hopkins University School of Medicine in Baltimore knew from other work that cells often use a molecule called LFA-1 to stabilize interactions mediated by cell-surface receptors. They report in the June 2 SCIENCE that LFA-1 plays a similar, critical role in the fusion of cellular membranes that follows cell attachment between HIV-infected and uninfected cells. When the scientists blocked the action of LFA-1 with antibodies, they prevented fusion of HIV-infected, cultured human cells.

Clinicians probably can't provide AIDS patients with large quantities of LFA-1 antibodies, because antibodies would block both useful and harmful actions of the multipurpose LFA-1 molecules. "You'd screw up too many things," says Richard O. Hynes of the Massachusetts Institute of Technology in Cambridge. However, he and Hildreth say, a limited course of LFA-1 antibodies may prove useful in AIDS patients undergoing an experimental therapy involving bone marrow transplants. While it's too early to tell, they say the antibodies may someday become part of a broader effort to keep new blood cells from becoming infected by residual, infected cells in the body.