COVID-19 infection alters kynurenine and fatty acid metabolism, correlating with IL-6 levels and renal status, 2020, Thomas et al

Open access, https://insight.jci.org/articles/view/140327/pdf

 

Well, well, well. Ain't that interesting?

 

A depletion of tryptophan and an increase in the kynurenine pathway. That seems part of a normal response to an infection.

But maybe, if the metabolic trap hypothesis is correct, and this particular virus provokes a particularly strong activation of the kynurenine pathway, then it could be good at causing the metabolic trap.

This part is also mildly interesting:

I'm too tired to read the entire article.

 

Ron Davis was measuring tryptophan in CELLS not in plasma.

 

Yes, much of this is known already and doesn't confirm the presence of a certain hypothesised metabolic trap.

 

No comments on it, but top of page 6 in the indented paragraph:

"Although no significant changes were noted in methionine levels, increases in acetyl-methionine and hydroxyproline, by-products of proteolysis and collagen catabolism, respectively, were observed, particularly in patients with COVID-19 with the highest IL-6 levels (Figure 4B). D"

and top of page 10:

"It is worth noting that proinflammatory signaling favors proteolysis and amino acid catabolism (represented herein by increased acetyl-methionine and hydroxyproline and altered levels of free amino acids), which can be antagonized, in part, by antiinflammatory cytokines (e.g., IL-37) (54) or inflammasome inhibitors (55)."

 

From the little I read of the paper (very little - I don't have the brain cells to make sense of it), it certainly seems quite a leap to draw the conclusions the twitter poster you quoted said @Trish