Katharina Buczek
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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