The paper Nadine Kabbani and I wrote in March/April got more traction today with this report in the FT (behind their firewall). Note that this latest original manuscript is actually still out to peer review at Altex, so please treat with caution.
But if Brain COVID19 were a thing, what might be going on? First, I think that the anosmia symptoms are pretty important here because olfactory odor receptors are actually part of the brain–the just hang out in your nose. If the virus gains access to the brain via those cells, then it potentially could use the wiring system of the nervous system as a superhighway. Second, the brain is actually separated from the rest of the adaptive immune system by the blood brain barrier. So virus in the brain can just chill–it’s not under constant attack from immune cells. The virus that causes Shingles actually does exactly this: after initially infecting a person (giving them Chickenpox), it awaits in neurons, for the right moment to reactivate. When it does, it produces the disease we know as Shingles.
What causes the reactivation? We don’t really know. And we have yet to see what a reactivated SARS-CoV2 might look like. I really hope we get a vaccine soon.