Recent Long COVID Research Found New Evidence That Points Toward The Cause Of Fatigue Syndrome
Even though COVID-19’s impact on school closures, small business struggles, supply chain shortages, and healthcare system deterioration may feel like a thing of the past, a significant number of adults are still fighting for their health in our post-COVID world.
According to the CDC, nearly one in five American adults who suffered from COVID-19 have been left with “long COVID syndrome” (LCS)– or symptoms that persist three or more months following infection.
In the wake of this widespread public health crisis, though, actually diagnosing and treating LCS remains very challenging since the underlying mechanisms that cause this disease are not very well understood.
One of the most prevalent symptoms of LCS, however, is fatigue. And researchers from the University of Vienna in Austria recently conducted a study that found new evidence regarding how fatigue is triggered following COVID-19 infection.
The team specifically used mass spectrometry-based post-genomic analysis, which allowed for conditions to be comprehensively mapped– or traced– within patient cohorts.
Primarily, when a viral infection is contracted and runs its course within the human body, the immune system usually experiences a strong activation.
Among virtually all of the LCS patients analyzed, though, the researchers found the opposite.
More specifically, classic inflammatory markers– including cytokines, eicosanoids, and acute phase proteins– were barely able to be detected.
And interestingly, this difference was even more substantial in LCS patients than among patients who were asymptomatic and recovering from the virus.
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“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.
So, even though this study was unable to answer all of the questions surrounding LCS, the team is confident that– equipped with these findings– new diagnostic options and monitoring methods will be offered to the public in the near future.
“The pathology of LCS disease is crystallizing more and more clearly, which of course, enables a completely new assessment of risk factors and therapy options,” the researchers underscored.
To read the study’s complete findings, which have since been published in iScience, visit the link here.
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