COVID-19 Spike Protein Causes Long-Lasting Blood Vessel Inflammation

Medical News: A new study from researchers at the University of Bern in Switzerland and Aarhus University in Denmark has shed light on how the SARS-CoV-2 spike protein causes prolonged inflammation in blood vessels. This discovery is crucial in understanding why some COVID-19 patients suffer from long-term complications, even after recovering from the acute phase of the disease. The study specifically explores the lasting effects of the spike protein on human endothelial cells, which are the cells lining the blood vessels, and how this could contribute to severe health issues such as blood clots and long COVID symptoms.

COVID-19 Spike Protein Causes Long-Lasting Blood Vessel Inflammation

How the Spike Protein Affects Blood Vessels
While COVID-19 is widely recognized for its impact on the lungs, evidence shows the virus can significantly affect the vascular system as well. The spike protein, the part of the virus that enables it to enter human cells, appears to have long-lasting inflammatory effects on the blood vessels. Researchers from both institutions explored this by isolating human endothelial cells from the aorta and lung microvascular systems and exposing them to the spike protein under laboratory conditions designed to mimic blood flow.
 
This Medical News report will provide insights from the study as to how the SARS-CoV-2 spike protein interacts with blood vessels, triggering prolonged inflammation that can lead to lasting damage. The findings of this study highlight the potential for these vascular changes to contribute to long-term complications in COVID-19 patients.
 
Endothelial Cells and Their Role in Vascular Health
Endothelial cells are the thin layer of cells lining blood vessels. They are responsible for maintaining smooth blood flow and regulating the movement of substances between the bloodstream and surrounding tissues. When these cells are damaged or inflamed, it can disrupt normal blood flow, leading to complications such as thrombosis (the formation of blood clots), tissue damage, and organ dysfunction.
 
In this study, the researchers discovered that exposure to the spike protein triggered a significant inflammatory response in these endothelial cells. Specifically, the cells showed increased production of adhesion molecules, which play a critical role in attracting immune cells to areas of inflammation. While this is a normal part of the body's defense against infection, the spike protein appeared to cause an extended inflammatory response that lasted long after the initial exposure.
 
Key Findings from the Study
The study team exposed endothelial cells from the human aorta and lung microvascular system to the spike protein. They observed the effects over 24 to 96 hours to determine how the protein influences cellular behavior. The results were striking: the spike protein caused a significant and prolonged increase in the production of adhesion molecules such as ICAM1 and E-Selectin. These molecules are essential for recruiting immune cells to areas of infection or damage.
 
This per sistent inflammatory response was comparable to the reaction caused by TNF-α, a cytokine known to induce strong inflammatory effects in the body. The researchers found that even after 96 hours, the levels of these adhesion molecules remained elevated, indicating that the spike protein has a long-lasting effect on blood vessel inflammation.
 
Chemokine Release and Coagulation State
In addition to the prolonged expression of adhesion molecules, the study also examined how the spike protein affected the release of chemokines - signaling molecules that attract immune cells to the site of infection or injury. The spike protein triggered the release of chemokines such as CXCL1, CXCL2, and IL-6, all of which play a role in the body's inflammatory response. This release continued over several days, suggesting that the spike protein can lead to an extended immune response in blood vessels.
 
Furthermore, the researchers discovered that the spike protein promoted a procoagulant state in the endothelial cells. This means that the cells became more prone to forming blood clots, a condition that has been frequently observed in severe COVID-19 cases. Even after the spike protein was removed, the procoagulant state persisted, raising concerns about the long-term risk of clotting disorders in patients who have recovered from the virus.
 
How This Relates to Long COVID
One of the most important implications of this study is its potential to explain some of the lingering symptoms seen in long COVID patients. Long COVID refers to the persistent symptoms experienced by some individuals long after they have recovered from the acute phase of the infection. These symptoms can include fatigue, chest pain, and shortness of breath. This research suggests that the spike protein may be contributing to these long-term symptoms by inducing chronic inflammation in blood vessels.
 
The sustained activation of adhesion molecules and chemokines means that the immune system could continue to target the body’s own tissues, even after the virus has been cleared. This prolonged immune activity may lead to damage in critical organs such as the heart, lungs, and kidneys, explaining why some individuals continue to experience health issues after their infection has resolved.
 
Implications for Treatment
The findings from this study underscore the importance of protecting endothelial cells during and after a COVID-19 infection. Since these cells are responsible for regulating blood flow and immune responses, their damage could have serious long-term consequences. Treatments aimed at protecting these cells and reducing the inflammatory effects of the spike protein could be key to preventing long-term complications in COVID-19 patients.
 
One potential therapeutic approach could involve developing drugs that specifically target the pathways activated by the spike protein. By blocking the inflammatory and procoagulant pathways triggered by the spike protein, it may be possible to reduce the risk of blood clots and other complications. Additionally, therapies that promote the healing and repair of damaged endothelial cells could improve outcomes for patients suffering from long COVID.
 
Conclusions
In conclusion, this study provides critical insights into how the SARS-CoV-2 spike protein affects blood vessels. The study demonstrates that the spike protein triggers prolonged inflammation and a procoagulant state in endothelial cells, which may contribute to long-term complications such as blood clots and organ damage.
 
These findings suggest that the vascular effects of COVID-19 extend beyond the acute phase of the disease and may play a significant role in the development of long COVID. Protecting endothelial cells and developing treatments that target the inflammatory pathways activated by the spike protein will be essential in mitigating the long-term effects of the virus.
 
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.researchsquare.com/article/rs-5003230/v1
 
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https://www.thailandmedical.news/news/australian-study-uncovers-covid-19-s-impact-on-the-endothelial-glycocalyx