After multiple failed attempts at developing a vaccine against one of the most common infections, Staphylococcus aureus, researchers at the University of California San Diego have suggestions about how to fix the problem.
Even with successful studies of a staph vaccine in mice, extending those same results have not been possible on the human side for decades, according to a Jan. 16 news release. But the decades of research into this aim have led UCSD researchers to test a new hypothesis about why it hasn't worked.
They set out to test whether Staph aureus bacteria could somehow trick the body to release antibodies that are non-protective, rather than ones that are. Since non-protective antibodies are preferentially recalled, the vaccines are then rendered ineffective, according to the study, which was published Jan. 16 in Cell Reports Medicine.
Testing this in mice, researchers found that vaccines were successful in the rodents that had never been exposed to the bacteria or to human antibodies against it, but if the rodents were exposed to one or the other prior to vaccination, this was not the case.
"One pathogen can have many different antigens that the immune system responds to, but there is a hierarchy as far as which antigen is dominant," Chih Ming Tsai, PhD, co-lead author of the study and project scientist in the Liu Lab at UCSD, said. "Most vaccines are based on the dominant antigen to trigger the strongest possible immune response. But our findings suggest that for SA, the rules are different, and it is more beneficial to target so-called subdominant antigens, which triggered a weak immune response in the first place."
This offers a path forward and "suggest[s] a whole new way of reevaluating failed vaccines, which could have implications well beyond this one bacterium," according to George Liu, MD, PhD, lead author, and professor at UC San Diego School of Medicine.
Further research and clinical trials in mice will still be necessary to test effectiveness of staph vaccines with this new model.