ABSTRACT
Although natural infection with HIV-1 induces a multiarmed immune response, including neutralizing antibodies, helper T cells (Th), and cytotoxic T lymphocytes (CTL) (1-8), this response is not usually sufficient to prevent the progression of HIV-1-mediated disease to AIDS and ultimately death. Therefore, for a vaccine to be successful, it will have to do better than natural infection at eliciting an adequate immune response. That such a response is possible is suggested both by the protective immunity achieved in monkeys using live attenuated simian immunodeficiency (SIV) vaccines (9-11) and by the small number of individuals who, despite normal chemokine receptors, appear to be resistant to multiple exposures to HIV-1 or who are long-term nonprogressors after infection (2,5,12-15). Furthermore, it is not surprising that a virus that evolves to escape the immune response of its host would not necessarily be the most potent vaccine for inducing immunity against itself. Thus, it should be possible to design a vaccine that is more effective at eliciting protective immunity than is the virus infection itself. The challenge is to design such a vaccine.
