by Allison Guy, All News Pipeline:

MIT Technology Review is a bimonthly magazine owned by the Massachusetts Institute of Technology. It focuses on science and technology.

Its latest issue features the work of Michal (“Mikki”) Tal, formerly of Stanford, now of MIT.

She started out researching immune responses to cancer, then began investigating Lyme disease. As the article describes it:

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In 2020, the pandemic slammed the brakes on most in-person research at Stanford, including Tal’s Lyme studies, and she switched to investigating the salivary immune response to covid…For Tal, the similarities with Lyme disease were uncanny. “Long covid looks exactly, and I mean exactly, like chronic Lyme,” she says. “One is caused by bacteria, and one is caused by a virus. And I started to ask myself this question: Does it matter which road you took to Rome? Or does it only matter that you’re in Rome?”

MIT immunoengineer Michal “Mikki” Tal remembers the exact moment she had an insight that would change the trajectory of her research, getting her hooked on studying a long-neglected disease that leaves millions of Americans suffering without treatment.

It was 2017, and she was a Stanford postdoc exploring connections between her immune regulation research and immuno-oncology, which harnesses the body’s immune system to combat cancer. Her work focused on how healthy cells broadcast “Don’t eat me” messages while cells that are cancerous or infected with a pathogen send self-sacrificing “Eat me” messages. Immune cells, in turn, receive these missives in pocket-like receptors. The receptor that receives the healthy cells’ signal, Tal read as she was poring over the literature that day, is the third most diverse protein in the human population, meaning that it varies a lot from one person to the next. It was a fact that struck her as “very odd.”

Tal, who has been obsessed with infectious disease since losing an uncle to HIV/AIDS and a cousin to meningococcal meningitis, wondered what this striking diversity could reveal about our immune response to infection. According to one hypothesis, the wide array of these receptors is the result of an evolutionary arms race between disease-causing microbes and the immune system. Think of the receptor as a lock, and the “Nothing to see here” message as a key. Pathogens might evolve to produce their own chemical mimics of this key, effectively hiding from the immune system in plain sight. In response, the human population has developed a wide range of locks to frustrate any given impostor key.

Wanting to test this hypothesis, Tal found herself walking the halls of Stanford, asking colleagues, “Who’s got a cool bug?” Someone gave her Borrelia burgdorferi, the bacterium that causes Lyme disease. Previous research from Tal’s collaborator Jenifer Coburn, a microbiologist now at the Medical College of Wisconsin, had established that Lyme bacteria sport a special protein crucial for establishing a lasting infection. Knock this protein out, and the immune system swiftly overwhelms the bugs. The big question, however, was what made this protein so essential. So Tal used what’s known as a high-affinity probe as bait—and caught the Borrelia’s mimic of our “Don’t eat me” signal binding to it. In other words, she confirmed that the bacteria’s sneaky protein was, as predicted, a close match for a healthy cell’s signal.

Be sure to also see this story from the Journal of Scientific Practice and Integrity titled “Long Before Suspicions Arose About A Lab Leak, Government Scientists Were Fiddling With Bugs to Make Them More Deadly.”

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