"Recently, we spent two years making an experimental outer coat vaccine candidate that had the correct areas on the outer coat for the good broadly neutralizing antibodies to bind to, and we vaccinated several kinds of animals. In none did we get any of the good antibodies. That frustrating result led me to ask if something was preventing these good antibodies from being made," Haynes said.
"A light went on when I saw that the rare human monoclonal antibodies had physical characteristics very similar to autoantibodies found in autoimmune disease ?in other words, to the antibodies the normal immune system does not allow to be made," Haynes said.
The results provide a new goal for future HIV research, Haynes said. "We can focus on trying to redirect the response to HIV outer coat proteins from innate B cells to adaptive B cells. Alternatively, we can develop ways to induce that first line of polyspecific antibody defense during vaccination, if these antibodies are not harmful to those being vaccinated," Haynes said.
"We now have a window into how to study HIV vaccines from the host side of the problem," he said.
Collaborators on the study include Judith Fleming, William St. Clair, Richard Scearce, Kelly Plonk, Herman Staats, Thomas Ortel, Hua-Xin Liao and Munir Alam of Duke; Herman Katinger, Gabriela Stiegler and Renate Kunert of the Institute of Applied Microbiology, University of Agriculture, Vienna, Austria; and James Robinson of the Tulane University School of Medicine. The National Institute of Allergy and Infectious Diseases of the National Institutes of Health supported the work.