Blood values ​​indicate reprogramming of immune cells

Long COVID study: Blood values ​​indicate reprogramming of immune cells

Clinical and epidemiological characteristics of a post-COVID-19 cohort. credit: Journal of Medical Virology (2022). doi: 10.1002/jmv.28364

The underlying mechanisms of prolonged COVID are not yet understood. Molecular evidence for different subsets of prolonged COVID has now been presented by a research group at University Medicine Halle.

When symptoms persist: After recovering from a COVID-19 infection, many people experience a secondary illness called prolonged COVID or post-COVID syndrome. A research group at University Medicine Halle has discovered molecular evidence for prolonged subtypes of COVID. Patterns occur that could provide a potential therapeutic approach.

The data indicate that various mechanisms lead to the development of the syndrome, including the ‘reprogramming’ of immune cells. All participants were recruited through “DigiHero”, a Germany-wide study of digital health research conducted by the University of Medicine Halle. The results were recently published in Journal of Medical Virology.

In the event of an infection, certain immune cells, called macrophages, form the first line of defense in the body’s immune response. They, along with their precursors, monocytes, are important cells of the innate immune system. They play an important role in activating and regulating the immune response by secreting immune factors as signaling molecules.

The research group from Hull, led by Professor Macha Binder, has already shown that the concentration of three of these immune factors rises in the blood of people with prolonged COVID symptoms. Until now, it was not clear to what extent the secretion of these factors was impaired, and it was hypothesized that viral remnants circulating in the blood during the acute phase of COVID-19 might influence the regulation of these immune cells.

Evidence for multiple subtypes of prolonged COVID

“Our study focused on other immune factors that promote inflammation and fibrosis that can be secreted by monocytes and macrophages,” explains Dr. Christoph Schultheis, lead author of the study and research associate at the IV Department of Internal Medicine at the University of Medicine Halle. “The release of these immune factors has been shown to be significantly dysregulated in prolonged COVID.” The scientists found that this “reprogramming” process occurred in two distinct molecular patterns.

In addition, blood levels of the viral spike protein S1, which the COVID-19 virus uses to infect cells, were examined. This protein was observed in some study participants after a COVID-19 infection, especially in those with prolonged COVID. However, these blood values ​​showed no association with dysregulated immune response patterns, as previously assumed. “This was a related finding that we interpreted as an indication of distinct subgroups of prolonged COVID that may result from divergent underlying mechanisms,” explains Schultheiss.

Individual symptoms do not allow conclusions to be drawn

It should also be noted that the detected subtypes appear to be independent of the symptoms of long-term COVID-19 patients. explains Professor Masha Binder, head of the research group and director of the IV Department of Internal Medicine.

“We were able to identify several immune factors in the blood and confirm the role they play in prolonged COVID. Treatment options already exist for some of these factors in order to counteract the dysregulation,” says Bender.

The published results were also based on the DigiHero study (www.medizin.uni-halle.de/digihero). DigiHero has already surveyed thousands of people across Germany about health-related issues via the digital platform. Professor Rafael Mikolajczyk of the Institute of Medicine, Epidemiology, Biometrics and Informatics at the University of Medicine Halle says.

more information:
Liquid Biomarkers of Macrophage Dysregulation and Disseminated Spiky Protein Biological Heterogeneity in Patients with Post-Acute Effects of COVID‐19, Christoph Schultheiss et al. Journal of Medical Virology (2022). doi: 10.1002/jmv.28364

Provided by the University of Medicine Halle

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