Preprint Immune Correlates of Hyperglycemia and Vaccination in a Non-human Primate Model of Long-COVID, 2023, Palmer et al

Immune Correlates of Hyperglycemia and Vaccination in a Non-human Primate Model of Long-COVID

Abstract
Hyperglycemia, and exacerbation of pre-existing deficits in glucose metabolism, are major manifestations of the post-acute sequelae of SARS-CoV-2 (PASC). Our understanding of lasting glucometabolic disruptions after acute COVID-19 remains unclear due to the lack of animal models for metabolic PASC.

Here, we report a non-human primate model of metabolic PASC using SARS-CoV-2 infected African green monkeys (AGMs). Using this model, we have identified a dysregulated chemokine signature and hypersensitive T cell population during acute COVID-19 that correlates with elevated and persistent hyperglycemia four months post-infection. This persistent hyperglycemia correlates with elevated hepatic glycogen, but there was no evidence of long-term SARS-CoV-2 replication in the liver and pancreas. Finally, we report a favorable glycemic effect of the SARS-CoV-2 mRNA vaccine, administered on day 4 post-infection.

Together, these data suggest that the AGM metabolic PASC model exhibits important similarities to human metabolic PASC and can be utilized to assess therapeutic candidates to combat this syndrome.

https://www.biorxiv.org/content/10.1101/2023.09.22.559019v1

 

"Hyperglycemia, and exacerbation of pre-existing deficits in glucose metabolism, are major manifestations of the post-acute sequelae of SARS-CoV-2 (PASC)." Apart from the Covid T2D link, I haven't seen evidence of this. But I suppose as long as Long Covid is very loosely defined one can almost claim anything.

This study also did an analysis of SARS-CoV-2 persistence in tissues 18 weeks post infection and the "data suggest no significant long-term persistence of replicating virus in the liver, pancreas or duodenum in our AGM PASC model".

 

When you have a million human subjects, why inflict this on some monkeys?

 

Not saying the above theory has any validity but presumably, if it were a common cause of ME/CFS, then UK GWAS (Chris Ponting - DecodeME) would turn up a genetic signal?