Why vaccines are not the answer – The failure of V520 and the importance of cell-mediated immunity in the fight against HIV

Abstract

The recent failure of Merck's HIV vaccine, V520, left the future of HIV vaccine research in question. The current article offers a possible explanation for the failure of V520 and explores a potential alternative to the vaccine approach. Vaccines prior to V520 were designed to evoke strong antibody-mediated immune responses to HIV; that is, the generation of antibodies to attach to and disable the HIV virus before it infiltrates host cells. V520 represents a misguided, though well-intentioned, effort to evoke a cell-mediated immune response to HIV; that is, immune activity aimed at identifying proteins associated with HIV after it infiltrates host cells. In the body, these two immune responses, antibody-mediated (for extracellular infections) and cell-mediated (primarily for intracellular infections), operate in a teeter-totter fashion. When one is activated the other is suppressed. Because HIV quickly infects host cells near entrances to the body, it requires a strong cell-mediated response to defeat, not an antibody-mediated response. The driving hypothesis of this article is that the antibody-mediated immune response triggered by V520 suppressed the ability of the body to mount the cell-mediated immune response necessary to protect against HIV and created a window of opportunity for HIV infection, particularly in subjects previously exposed to the adenovirus vector used in the vaccine. While the immune system uses antibodies to identify extracellular pathogens, it uses transfer factors to label infected host cells. Hundred of papers indicate that pathogen-specific transfer factors can be used to stimulate cell-mediated immunity against a wide variety of viruses. The available research, reviewed in this manuscript, suggests that HIV-specific transfer factors could prove extremely useful, far more useful than vaccines, in preventing and treating HIV infections.