Tests in mice indicate that the bacterium that causes Lyme disease can commandeer a gene in its interim host—the deer tick—enabling the bacterium to escape immune detection once inside a mammal.
Researchers at Yale University report in the July 28 Nature that the Lyme microbe, Borrelia burgdorferi, activates a gene in the tick, boosting production of a salivary protein called Salp-15.
Conveniently for the bacterium, it can bind to this protein, Yale microbiologist Nandhini Ramamoorthi and her colleagues note. When a tick bites a person or another mammal, the Salp-15-coated bacteria enter through the skin, she says.
The coating apparently renders B. burgdorferi at least partially invisible to mammalian immune cells, she says. That buys precious time for the microbes to multiply in the skin and then spread to other organs. In persons with advanced Lyme disease, the bacteria cause nervous system and joint damage.
It remains unclear how B. burgdorferi activates the tick gene encoding Salp-15 or why the immune system doesn’t detect the microbe once it’s coated, Ramamoorthi says.
If scientists can devise antibodies to Salp-15, they might be able to stop B. burgdorferi from inflicting any harm beyond the site of the bite, she says.