"We saw this same pattern across all human #COVID lung samples," Wernig said. As with other #lung infections, the initial #COVID19 infection in the lungs kicked off an #inflammatory process. In the case of #LongCovid patients, however, the #immune dysfunction keeps going long after the virus is gone -- similar to what happens in chronic #PulmonaryFibrosis.”
Back to back days that two separate institutions claim to have figured this out, but with what appear to be different meechanisms.
That's fair. Re-reading what I wrote I want to make clear I wasn't saying "Someone's lying!"
I'm a big proponent of "There's a lot of different things going on" whenever someone is waiting for the single treatment that will solve all of the COVID problems. I meant it more like "Lots going on here."
Re-reading I can also see that I misspelled mechanisms. Oof.
@BE it’s mastodon… I _love_ the edit. 👏
@BE I would see these as complimentary “Unique monocyte profiles distinguished long COVID patients with shortness of breath and unresolved lung injury from those with ongoing fatigue, and from asymptomatic patients.”
I.e. there are immunological shenanigans at play. (Which was the gist of the fibrosis article).
Takes me back to when someone posted about low cortisol found in long COVID. Again that was likely the outcome/surrogate marker, not the underlying pathology.
Nasty nasty virus.