JON KRAUSEAt the beginning of 1991—almost ten years after the cause of AIDS had been identified—researchers thought they might have a vaccine. Evidence from several laboratories suggested that it was possible to develop a vaccine against HIV by inoculating individuals with a crippled version of the virus that could not replicate—a time-tested strategy similar to that used to produce effective measles, mumps, and polio vaccines. In animal experiments, researchers used an HIV-like virus called simian immunodeficiency virus (SIV) which infects rhesus macaque monkeys. Over time, infected monkeys developed AIDS-like symptoms, much like humans. Researchers inactivated SIV, injected it into monkeys, and tested whether the animals were protected against live SIV infection. Most vaccinated monkeys were indeed protected, encouraging AIDS researchers to believe that an effective human AIDS vaccine would soon follow.
However, in October 1991, a brief article was published that sent AIDS vaccine research into a tailspin.[1. E.J. Stott, “Anti-cell antibody in macaques,” Nature, 1991, 353:393, 1991.] Like other labs,[2. E.J. Stott, G.C. Schild, “Strategies for AIDS vaccines,” J Antimicrob Chemother, 37 Suppl B:185-98, 1996.],[3. T. Lehner et al., “Alloimmunization as a strategy for vaccine design against HIV/AIDS,” AIDS Res Hum Retroviruses, 16:309-13, 2000.] E. James Stott’s laboratory had immunized macaques with inactivated SIV, which protected them against subsequent infection with live virus. However, the Stott laboratory included a negative control that was missing from the earlier studies: a second group of monkeys was immunized with just the human host cells that had been used to grow the inactivated SIV, but in this case, with ...
