- SARS-CoV-2, the virus that causes COVID-19, can produce short- and long-term symptoms.
- Researchers of a new study found that amyloids are the abnormal proteins which are also known to cause Alzheimer’s could arise during SARS-CoV-2 infection, which could explain some of the symptoms experienced.
- Research suggests that the immune system may interact with SARS-CoV-2 This leads to the production of these misfolded spike proteins, leading to blood clots and neurological symptoms.
The cause of the many mysterious and persistent symptoms caused by SARS-CoV-2 infection, or COVID-19, remains an elusive mystery for scientists. Researchers have looked at different systems in the body to find answers.
A sometimes controversial area of study has been microclots in people with long COVID, caused by fibrin, a substance that helps blood to clot. This has made both the immune and circulatory systems interesting candidates for further study.
A recent study published in Journal of the American Chemical Societyhas provided a proposed mechanism to explain why some people develop complicated COVID-19 symptoms after infection.
The results suggest that some persistent COVID-19 symptoms may be related to amyloid production caused by the immune system interacting with the S protein (spike protein) on the surface of the SARS-CoV-2 virus .
For example, amyloid deposits are present in conditions such as Alzheimer’s disease, a condition that affects thinking and memory. But certain amyloids are also associated with several others
- cardiac arrhythmias
- Type 2 diabetes mellitus
- Rheumatoid arthritis
Research on how amyloids affect the body is ongoing. One area of interest is how amyloid production may be related to severe COVID-19 cases and the symptoms we see in people with long COVID.
SARS-CoV-2 can cause a wide variety of symptoms in individuals, and researchers do not fully understand why these symptoms occur in some people or affect them more than others.
In the present study, the researchers wanted to investigate whether the spike protein in SARS-CoV-2 could be converted into amyloids in the body. The spike protein
The researchers found that several components of S protein could potentially produce amyloids.
The authors of the study note that the S protein alone would probably not break down into amyloid. They theorized that in order for amyloid to form, the S protein would have to react with something, such as an enzyme that breaks down the S protein into smaller components.
When they combined the S protein with neutrophil elastase in vitro – a proteolytic enzyme (protease) produced in the human body by a type of white blood cell released early in SARS-CoV-2 infection called neutrophils – the researchers found that the S-protein breaks down into sections that could lead to amyloid production.
They also found that combining the S protein with the protease of neutrophil elastase formed amyloid-like fibrils.
Other research in this study looked at the relationship between S protein and blood clot formation. Study author Sophie Nystrom explained this Medical News Today:
“Under normal circumstances, when we get an injury, the fibrinogen that we have in our bloodstream is converted to fibrin to form clots. To prevent ‘over-clotting’ there is another blood component, plasmin, which dissolves the fibrin clots when there are enough, and ultimately gets rid of all the fibrin when it is no longer needed.”
“Our experiment shows that when fibrin is formed in the presence of spike amyloid, the plasmin cannot completely clear the fibrin clots,” Nystrom added.
Overall, the study opens further speculation about how SARS-CoV-2 interacts with the body to bring about certain health problems and symptoms.
For example, it’s possible that amyloid production could contribute to some of the symptoms we see with COVID-19, like blood clots and neurodegenerative problems.
dr Arturo Casadevall, an infectious disease expert at Johns Hopkins University in Baltimore who was not involved with the study, was intrigued by the study’s findings.
“This is a very interesting study showing that the SARS-CoV-2 spike protein has domains that could promote aggregation to form amyloid fibrils. Such fibrils have been linked to cellular dysfunction, and if this had happened during COVID-19 it would suggest another mechanism by which the virus can damage organs,” he said MNT.
“Our finding that the SARS-CoV-2 spike protein can form amyloid when cleaved by neutrophil elastase is likely an important piece of the puzzle for many unsolved questions related to COVID-19 infection.”
— Sophie Nystrom, author of the study
The study had several limitations. For example, it was an in vitro study, so there’s still a lot of unknowns about how this finding relates to what’s happening in the human body. There may also be other factors that contribute to amyloid formation.
“It is important to emphasize that this is an in vitro study and that we have no evidence that the phenomenon occurs during COVID-19 or that it contributes to the pathogenesis of the disease. But the importance of the work is that it opens up a new possibility that scientists can now investigate if it is relevant to the disease,” warned Dr. Casadevall.
dr Casadevall also expressed skepticism that amyloid production is the cause of the neurological side effects seen in people with COVID-19.
“To conclude that these amyloid structures are responsible for the neurological effects is too speculative at this time, simply because there is no evidence that such structures are produced during human infection,” he said.
The results also do not suggest that experiencing COVID-19 increases a person’s risk of developing dementia. However, the study offers a promising starting point for further research into the underlying causes of COVID-19 symptoms and their long-term health effects.