Katharina Buczek
“This finding shows that there was indeed some residual inflammatory response detectable in asymptomatic recovered patients, whereas long COVID patients had the opposite finding,” explained Christopher Gerner, one of the study’s authors.
So, even though it was previously believed that auto-immunity was the leading cause of LCS, these findings indicate that there is no evidence of LCS patients experiencing an accompanying inflammatory response.
Instead, the researchers actually uncovered numerous anti-inflammatory lipids, proteins, and metabolites among LCS patients– a finding which points to two possible scenarios.
First, they may contribute to some of the most significant LCS symptoms. Or, they may point toward macrophage polarization as the actual cause.
Again, Gerner detailed how these mechanisms may contribute to LCS symptom onset– specifically fatigue.
“The molecular signature of inflammation inhibition was very clearly visible. For instance, the study provides evidence that increased infectivity of the virus can be explained via a deficiency of acute phase proteins,” he said.
“In addition, the researchers were able to show that the anti-inflammatory metabolites osmolytes taurine and hypaphorine were strongly upregulated in LCS patients.”
And since hypaphorine has been found to induce sleep spontaneously in animals, this suggests that there is a direct link to fatigue syndrome.
Analyzing the blood plasma of LCS patients also allowed the research team to gain deeper physiological insights.
More specifically, it was found that the active participation of alternatively polarized macrophages became more apparent.
These are cells that typically form after various kinds of infections and are primarily responsible for regenerative processes.
