May 14, 2004

Study finds HIV protein can drive immune cells away

MGH researchers may have provided another clue as to how HIV, the virus that causes AIDS, evades the immune system's defenses. In the May issue of the Journal of Virology, a team from the Partners AIDS Research Center (PARC) at the MGH describes how a key protein that helps the virus enter its target T helper cells may also keep away the T killer cells that should destroy HIV-infected cells. "We have identified a potential new mechanism by which pathogens can repel immune cells and thereby evade the immune system,"says Mark Poznansky, MD, PhD, of PARC and the MGH Infectious Disease Unit, the paper's senior author.

In 2000, Poznansky and colleagues found that a protein known to attract immune cells can actually repel T cells when present in elevated quantities. Because that molecule is known to interact with a receptor also used by HIV when it enters T helper cells, it seemed a logical next step to investigate whether HIV infection involves the same kind of cellular repulsion observed in the earlier study — a process the researchers dubbed "fugetaxis." A series of experiments led by research fellow Diana Brainard, MD, verified that the interaction of the HIV protein gp120 with the T cell receptor called CXCR4 can influence immune cell movement and at higher concentrations can repel immune cells.

"We don't know yet if this process occurs in patients infected with HIV, but if it does, it provides a new therapeutic approach that could block this viral protein activity and allow immune cells to do their job," Poznansky says.

Other MGH/PARC authors of the study are William Tharp, Elva Granado, Nicholas Miller, Alicja Trocha and Bruce Walker, MD.