Learning from past failures in the development of staph vaccines may inform how other vaccines for common bugs should be developed
Our skin is crawling with Staphylococcus aureus, the bacterium responsible for most staph infections. Usually staph is harmless, but sometimes—if it breaks through the barrier of our skin or hitches a ride on our food—it can cause severe rashes, food poisoning and even death. For more than a century researchers and clinicians have attempted to find a way to vaccinate against staph infections to no avail. Now researchers point to one possible explanation: staph knows us all too well.
That is an intriguing idea. But exploring this hypothesis in human experiments turns out to be a tough proposition because many of us are too contaminated to make good test subjects. “One out of three of us are colonized with staph,” Liu says, and nearly 50 percent of human babies are colonized in the first two months of life.
Injecting one set of mice with a salt solution while injecting another group with live staph in the weeks before vaccination allowed the researchers to compare different levels of vaccine efficacy in the two groups. When the disease-free mice were vaccinated, “it was hugely successful,” Liu says. But in mice that had previously had staph, “the vaccine didn’t work at all,” he says. “In fact, what was so surprising was [the efficacy] was a flatline. It did not work. It was 0 percent.
The culprit seems to be the immune system’s memory of the nonprotective antibodies, which counteracts any positive effect of the vaccine antibodies. This gives staph a two-pronged way of evading the immune system. “[The first] is bringing back the bad antibody, which prevents a lot of good antibodies from forming,” Liu says, “And the second step is: you could have bad antibodies further crowd out and actually outcompete the good antibodies, so they don’t work.
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