Meanwhile, recent work with another disease strikingly similar to the plague, AIDS, suggests O'Brien was on the right track. HIV, the virus that causes AIDS, tricks the immune system in a similar manner as the plague bacterium, targeting and taking over white blood cells. Virologist Dr. Bill Paxton at the Aaron Diamond AIDS Research Center in New York City noticed, "the center had no study of people who were exposed to HIV but who had remained negative." He began testing the blood of high-risk, HIV-negative individuals like Steve Crohn, exposing their blood to three thousand times the amount of HIV normally needed to infect a cell. Steve's blood never became infected. "We thought maybe we had infected the culture with bacteria or whatever," says Paxton. "So we went back to Steve. But it was the same result. We went back again and again. Same result." Paxton began studying Crohn's DNA, and concluded there was some sort of blocking mechanism preventing the virus from binding to his cells. Further research showed that that mechanism was delta 32.
Scientists studying HIV first learned about the gateway-blocking capacity of the CCR5 mutation in 1996. Several drug companies, then, quickly began exploring the possibility of developing pharmaceuticals that would mimic delta 32 by binding to CCR5 and blocking the attachment of HIV. Previous methods of treatment interfered with HIV's ability to replicate after the virus has already entered a cell. This new class of HIV treatment, called early-inhibitor -- or fusion-inhibitor -- drugs seek to prevent the virus from ever attaching at all. These pharmaceuticals are still in relatively early stages of development, but certainly stand as a hopeful new method of approaching HIV treatment
