Her doctors diagnosed a dangerous condition called acute necrotizing hemorrhagic encephalopathy, or ANE, which they detailed in the journal Radiology last month. It’s a rare complication known to occasionally accompany influenza and other viral infections, though usually in children. With the flu, scientists believe such brain damage is caused not so much by the virus itself but by squalls of inflammation-inducing molecules called cytokines, which are sometimes produced in excess by the body’s immune system during an infection. Scientists are still trying to figure out if the same is true for Covid-19, or if the coronavirus called SARS-CoV-2 is actually invading the nervous system directly. It’s an open question, the answer to which could have wide-ranging implications for how doctors diagnose and treat Covid-19 patients.

BUT IF SARS-COV-2 turns out to be a brain-invader, it wouldn’t shock Stanley Perlman, a microbiologist and infectious disease physician at the University of Iowa. During the 2003 SARS epidemic that killed 774 people, only a few dozen autopsies were ever performed. But in at least eight of them, pathologists found bits of the virus and its genome in the brain, in addition to the lungs, kidneys, digestive tract, and spleen. Perlman wanted to understand how that might happen. So he zoomed in on a receptor called ACE2, which SARS-CoV—the coronavirus that causes SARS—uses to enter human cells. In a 2008 study, Perlman and his colleagues genetically engineered mice to express that human receptor and then squirted a small dose of SARS-CoV into their noses. Rather than descending into their lungs, the virus climbed out of the nasal cavity and into their brains using olfactory neurons like rungs on a ladder.