At 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. Like other labs,
, 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 no trace of the virus.
1 The purpose of this negative control was to ensure that the immune reaction that had successfully protected the monkeys was specific to SIV antigens, and not induced by something else. Surprisingly, the “negative control” produced protective immunity against SIV infection. Equally surprising was the fact that protection in the vaccine group was not associated with antibodies that recognized SIV antigens.
The finding was viewed by most in the field as an artifact and in the years that followed, researchers continued to focus on developing vaccines against HIV that specifically targeted proteins on the surface of the virus. However, HIV proved to be a moving target, avoiding vaccine-induced immune responses by rapidly mutating its surface proteins, and thereby thwarting this type of virus-specific vaccine effort...
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