We have hypothesized and have presented evidence that there may be another form of immunity, other than humoral and cellular immunities, which operates against retroviruses. In order to distinguish it from the traditional immune responses, we have named this form of immunity "molecular immunity". The major goal of this hypothesis is to better define the "messenger molecules" that are critical in forming the molecular immunity against retroviruses, and to further determine the activation pathways of this relatively unexplored form of immunity. We have provided evidence that this natural immunity against retroviruses and specifically against HIV-1, can be activated and optimized, and have made some interesting observations. We believe that resistance to HIV-1 and to other retroviruses can be induced by various means, including low dose exposure, infection with replication defective viruses and exposure to non-pathogenic but genetically related viruses.