Neuropathology and virus in brain of SARS-CoV-2 infected non-human primates, 2022, Rutkai et al

[Sly Saint]

Abstract


Neurological manifestations are a significant complication of coronavirus disease (COVID-19), but underlying mechanisms aren’t well understood. The development of animal models that recapitulate the neuropathological findings of autopsied brain tissue from patients who died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are critical for elucidating the neuropathogenesis of infection and disease. Here, we show neuroinflammation, microhemorrhages, brain hypoxia, and neuropathology that is consistent with hypoxic-ischemic injury in SARS-CoV-2 infected non-human primates (NHPs), including evidence of neuron degeneration and apoptosis. Importantly, this is seen among infected animals that do not develop severe respiratory disease, which may provide insight into neurological symptoms associated with “long COVID”. Sparse virus is detected in brain endothelial cells but does not associate with the severity of central nervous system (CNS) injury. We anticipate our findings will advance our current understanding of the neuropathogenesis of SARS-CoV-2 infection and demonstrate SARS-CoV-2 infected NHPs are a highly relevant animal model for investigating COVID-19 neuropathogenesis among human subjects.


https://www.nature.com/articles/s41467-022-29440-z

 

[Jonathan Edwards]

Perhaps further evidence to support the hypothesis that playing with viruses in labs with poor safety standards is not such a good idea.

 

[Jonathan Edwards]

And of course passing the same virus through another non-human host is an ideal way to create new variants that might be 100 times more lethal.

...
Long time passing.
When will they ever learn,
When will they ever learn?

 

[Hutan]

Neuronal degeneration and activation of caspase 3 observed in this study supports this notion and indicates non-reversible neuronal injury may be significant to individuals suffering from PASC. Finally, our findings and conclusions presented herein suggest the need for long-term neurological follow-up of persistently symptomatic convalescent patients.

Well, that's progress, suggesting people with ongoing symptoms should have neurological investigations. While 'non-reversible neuronal injury' may account for some lingering and even permanent post-infection symptoms, I'm not sure that it explains the fluctuating brain fog of ME/CFS. Perhaps, as a result of a one-hit neuronal injury, our brains have to work harder even just to have a conversation, and so exhaustion rapidly sets in? I'm not terribly convinced that that is the whole story.

Together, our findings demonstrate scarce SARS-CoV-2 infection in brain-associated endothelial cells in deep brain structures of NHPs, even in the absence of severe disease or overt neurological symptoms.

These monkeys were killed before they had a chance to exhibit anything like Long Covid. This study suggests viral persistence in the endothelium of the brain might be possible.

I'd prefer that monkeys were left alone, and instead the brains of people who have died after having a Covid-19 infection but who didn't die of the Covid infection - both people who recovered fully and people who developed Long Covid - were looked at very carefully. Maybe we need to write to brain banks to try to convince them that they may have a key role in working out what is going on in Long Covid and ME/CFS.