Illustration by Garry Marshall

(Left) HIV muscles its way into cells by first attaching to a cellular receptor called CD4 and then to another receptor called CCR5. (Right) A new drug to treat AIDS blocks CCR5 to stop HIV from fusing with human cells.

AIDS drugs have always shared one trait: They disable HIV by knocking out several of its enzymes. But the virus is so sneaky, it can foil those medications by mutating. Now a new class of drugs attacks the virus in a different way-by protecting the cells that host it.

The idea for these new treatments emerged about five years ago when scientists discovered that HIV attaches itself to more than one cellular receptor when invading the body’s immune cells. The virus has long been known to clamp on to a receptor called CD4, but several common strains must also attach to a co-receptor called CCR5. The importance of CCR5 soared when further research revealed that some people (about 1 percent of northern Europeans) lack a chunk of the two genes that make it-and those people tend not to contract HIV. (Some researchers speculate that this gene variation occurs more often in Europeans because it made their ancestors resistant to bubonic plague.)

Scientists were thrilled. “We knew we could find a drug that does what some people do naturally,” says Robert Consalvo of pharmaceuticals giant Schering Plough. The first of the new drugs (currently known as SCH-C) works by attaching to CCR5 and blocking the virus from the cell. In an early trial, the drug was given to 12 people and reduced the amount of virus in their bloodstreams at least fivefold.

Clinical trials should be complete within five years. But even if the drug proves effective, the virus could still mutate and learn to latch on to some other receptor. Consequently, says Consalvo, it will be given as part of a multi-drug cocktail.