Ask Stephanie Moquin why she fell in love with viruses as an undergrad, and you might just fall in love with them yourself. Our bodies are teeming with them. Our genomes are partially built from their ancient remains. And they can seem like molecular magicians: “They can do so much with so little,” Moquin said. “You know, some viruses are like 10 genes, and they’re able to hijack a whole cell and make a bunch of copies of themselves.”
Like so many in biomedicine, Moquin now spends her days figuring out how to destroy the object of her fascination. In the spring of 2020, she’d just finished up a project on killing the virus that causes dengue fever. “I was literally like, ‘What should be doing next?’” she said.
The answer arrived in the form of a pandemic. By sifting through enormous libraries of molecules, Novartis found a few possibilities that looked like they might disrupt the new coronavirus — and potentially coronaviruses writ large.
They all glom onto a particular protein that’s a bit like a pair of scissors. In order to replicate itself, the virus has an inner copying machine of sorts, which is stored in pieces, its components encased in packaging. Getting the machine assembled and working involves cutting open the casing and springing out the necessary building blocks. You can imagine this potential drug as blocking the molecular scissors: If you can’t cut through the packaging, you can’t put together the copy machine, and if you can’t put together the copy machine, you can’t churn out more and more virus.
Her team hopes to start clinical trials next year. She also hopes that other antivirals that work in different ways might be used as a cocktail. “What we’re probably going to see is resistance emerging against an antiviral, like we always do,” Moquin explained. “If we could nip it in the bud and do a combination, early, from the very beginning, and we would never get any resistant viruses — that’d be really exciting.”
— Eric Boodman
