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Comparable Immune Alterations and Inflammatory Signatures in ME/CFS and Long COVID
Steliyan Petrov1, Martina Bozhkova1, Mariya Ivanovska1
1Department of Medical Microbiology and Immunology "Prof. Dr. Elissay Yanev", Medical University of Plovdiv, 4002 Plovdiv, Bulgaria.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID share similar immune biomarker profiles, including reduced lymphocytes and elevated pro-inflammatory cytokines. No significant differences were found between these conditions in the study.
Area of Science:
- Immunology
- Post-viral Syndromes
- Chronic Illness
Background:
- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex illness with debilitating fatigue and multisystemic symptoms.
- Long COVID, a post-viral syndrome from SARS-CoV-2 infection, presents overlapping clinical features with ME/CFS.
- Both conditions involve chronic immune activation, suggesting potential shared immunopathological mechanisms.
Purpose of the Study:
- To compare immune biomarkers in patients with ME/CFS and Long COVID against healthy controls.
- To investigate the immunopathological overlap between ME/CFS and Long COVID.
Main Methods:
- Analysis of lymphocyte subsets and cytokine profiles in 190 participants (65 ME/CFS, 54 Long COVID, 70 healthy controls).
- Assessment of psychological status and its correlation with immune markers.
Main Results:
- Both ME/CFS and Long COVID groups exhibited significantly lower levels of lymphocytes, CD8+ T cells, and NK cells compared to healthy controls.
- Elevated levels of pro-inflammatory cytokines (IL-6, TNF, IL-4, IL-10) were observed in both ME/CFS and Long COVID patients relative to controls.
- No statistically significant differences in the measured immune biomarkers were detected between the ME/CFS and Long COVID groups.
Conclusions:
- ME/CFS and Long COVID demonstrate comparable immune and inflammatory profiles.
- The findings suggest a shared immune dysfunction underlying both conditions, irrespective of the initial trigger.
- Further research into these shared mechanisms could inform therapeutic strategies for both post-viral syndromes.
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