Autoantibodies Targeting Endothelin Type A Receptor Possibly Behind Orthostatic Intolerance in Long COVID
Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 19, 2025 1 day, 18 hours, 40 minutes ago
Medical News: Shedding Light on a Lingering Mystery
Long COVID has emerged as a complex and perplexing condition, affecting millions worldwide. One of its persistent and troubling symptoms is orthostatic intolerance, a condition in which individuals experience dizziness, rapid heartbeat, and other symptoms upon standing. Scientists at the Medical University of Vienna in Austria have now identified a potential culprit: autoantibodies targeting the Endothelin Type A Receptor (ETAR). Their research suggests that these autoantibodies may contribute to endothelial dysfunction, which could explain the vascular and autonomic issues seen in long COVID patients.
Autoantibodies Targeting Endothelin Type A Receptor Possibly Behind Orthostatic Intolerance in Long COVID
Understanding Autoantibodies and Their Role in Long COVID
Autoantibodies are proteins produced by the immune system that mistakenly attack the body's own tissues. In long COVID, these rogue antibodies have been implicated in various symptoms, including neurological issues, chronic fatigue, and cardiovascular complications. This
Medical News report examines a recent study that specifically explores how ETAR autoantibodies might be disrupting normal blood flow and autonomic regulation in affected individuals.
The study, conducted by researchers from the Medical University of Vienna, involved 100 long COVID patients from their POSTCOV registry. These patients were compared to three control groups: individuals who had recovered from COVID-19 without lingering symptoms, vaccinated individuals with no history of infection, and healthy unvaccinated individuals who had never contracted COVID-19. The results pointed to significantly higher levels of ETAR autoantibodies in long COVID patients, particularly those experiencing orthostatic intolerance.
Key Findings: A Strong Link Between ETAR Autoantibodies and Orthostatic Intolerance
The researchers found that ETAR autoantibody concentrations were markedly elevated in long COVID patients when compared to those who had never encountered the SARS-CoV-2 virus. Even vaccinated individuals without prior infection showed increased levels of these autoantibodies, indicating that exposure to the spike protein - either through infection or vaccination - could play a role in their development.
Interestingly, while ETAR autoantibodies were notably higher in long COVID patients, other autoantibodies, such as those targeting beta-2 adrenergic receptors (Beta-2 AR) and Angiotensin 1-7 (Ang1-7), showed only moderate increases. This suggests that ETAR may play a more central role in the vascular dysfunction seen in long COVID than other known autoantibody targets.
The Impact on Quality of Life
The study also found that ETAR autoantibody levels correlated strongly with patients’ reported difficulty in carrying out daily activities. Using the EQ-5D questionnaire, a standardized measure of health-related quality of life, researchers discovered that higher levels of ETAR auto
antibodies were associated with greater impairment in routine activities such as work, household tasks, and personal care.
Implications for Treatment and Future Research
These findings open the door for new therapeutic approaches. If ETAR autoantibodies are indeed driving the symptoms of orthostatic intolerance in long COVID, treatments that target these antibodies or the pathways they affect could offer relief. Potential strategies might include immunomodulatory therapies, such as intravenous immunoglobulin (IVIG) or monoclonal antibodies, designed to neutralize harmful autoantibodies.
Additionally, researchers suggest that medications targeting the endothelin pathway, such as endothelin receptor antagonists (ERAs), could be investigated for their potential benefits in treating long COVID symptoms related to vascular dysfunction.
The Broader Picture: Autoimmunity and Long COVID
This study is part of a growing body of evidence that long COVID has significant autoimmune components. Other studies have previously identified autoantibodies targeting various receptors involved in cardiovascular and neurological regulation. The presence of these autoantibodies may explain why some long COVID patients experience symptoms that resemble conditions such as postural orthostatic tachycardia syndrome (POTS) and chronic fatigue syndrome (CFS).
Limitations and Future Directions
While the study provides compelling evidence of a link between ETAR autoantibodies and orthostatic intolerance, further research is needed to fully understand the mechanisms at play. One limitation is that the study was observational, meaning it can demonstrate correlation but not causation. More extensive studies, including interventional trials, will be necessary to determine whether reducing ETAR autoantibody levels can lead to symptom improvement.
Additionally, researchers acknowledge that long COVID is a highly heterogeneous condition, meaning that not all patients will have the same underlying causes for their symptoms. Future research should aim to identify subgroups of patients who might benefit most from targeted autoimmune therapies.
Conclusion: A Step Toward Understanding and Treating Long COVID
The discovery of elevated ETAR autoantibodies in long COVID patients represents an important step toward understanding the condition’s underlying mechanisms. The correlation between these autoantibodies and orthostatic intolerance symptoms provides a potential biomarker for identifying affected individuals and developing targeted treatments. While much work remains to be done, this research offers hope for millions of long COVID sufferers struggling with daily symptoms and an uncertain future.
The study findings were published in the peer-reviewed journal: Biomolecules.
https://www.mdpi.com/2218-273X/15/2/300
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