HIV, the AIDS-causing virus, is a master of eluding the body’s immune system – in part because it targets cells of the immune system itself as part of its reproductive strategy. This makes development of vaccines to protect against HIV especially difficult, because vaccines require a functioning immune system in order to work. If HIV escapes early immune system defenses, later defenses may fail.
The first modestly encouraging clinical trial of an anti-HIV vaccine was announced two years ago. Frustratingly, however, it was not clear how the vaccine involved actually worked.
Scientists are still studying blood samples from trial participants to search for differences that might explain why the vaccine worked for some but not for others. So far two antibodies have been identified that target different HIV antigens – one antibody that is associated with more successful results, and the other with less successful ones. These are the first clues ever found that seem to point towards a successful HIV vaccine mechanism.
Barton Haynes, the director of the Duke Human Vaccine Institute in Durham, North Carolina, who coordinated the follow-up study, said at a press conference that the results will generate hypotheses for further study. “What we now have are clues as to why it might have worked. That’s something we haven’t had over the past 30 years. That’s very important for the field.”
Researchers are already planning to test whether antibodies like those found in trial participants have the same effect in primates infected with a virus related to HIV. These experiments will determine whether these immune responses are responsible for the vaccine’s success or failure in particular people or merely linked to other underlying factors.