The Duke team discovered that certain broadly protective antibodies, which recognize and latch onto the HIV protein gp41, resemble antibodies made in autoimmune diseases. In most people, the immune system destroys these types of antibodies to prevent attacks against self.
The Duke study suggests HIV vaccines may have failed in part because certain proteins on HIV's protective outer coat trigger only short-lived, self-reactive antibodies instead of long-lasting, HIV-specific antibodies. The results also imply that during the initial infection stage in humans, HIV may escape destruction by the immune system because these seemingly vulnerable outer coat proteins activate self-reactive antibodies.
"The fundamental problem in all of HIV vaccine research has been that when you inject the envelope of the HIV virus into people or animals, no broadly neutralizing antibodies ?those antibodies that kill most HIV strains ?are made. This provides a plausible explanation for why broadly protective antibodies have not been made in response to currently tested HIV vaccines," said Barton Haynes, M.D., lead author of the study and director of the Human Vaccine Institute at Duke University Medical Center.
The researchers will report their findings in a forthcoming issue of Science. The results were published online April 28, 2005, in Science Express.
The antibody-producing portion of the human immune system is broadly divided into two categories. The first, innate B cell immunity, comprises fast-acting but weak antibodies that fight a broad range of pathogens. These antibodies can also attack the body itself, as in autoimmune disorders