(ORDO NEWS) — Bleeding disorders are one of the most common symptoms of Covid-19 in patients with severe and prolonged illness.
In a new study, scientists from Sweden have found that our immune system may be responsible for this, thereby playing against us.
By destroying the SARS-CoV-2 virus, immune cells simultaneously contribute to the formation of amyloids, cleavage-resistant branched proteins that can lead to neurological and cardiovascular diseases, as well as increase the risk of developing diabetes.
Despite the prevalence of coronavirus infections, before SARS-CoV-2, no viruses were known that would cause such a wide variety of severe symptoms, affecting many other internal organs in addition to the lungs.
Severe Covid-19, along with acute respiratory distress syndrome resulting from inflammatory reactions of the innate immune system that cause damage to the lungs, can also lead to cytokine storm, heart damage (including inflammation of the heart muscle), kidney damage, neurological disease, damage circulatory system leading to impaired blood flow.
In addition, persistent emotional illnesses and mental health conditions that resemble neurodegenerative diseases are possible.
Why Covid-19 affects the body in this way remains largely a mystery. However, in a new study, scientists from the University of Linköping,
Sweden seem to have identified a biological mechanism that has not been previously described anywhere and which may be part of the explanation of this mystery.
The research team is studying diseases caused by misfolded proteins, or amyloids, the best-known examples of which are Alzheimer’s disease and complications of type 2 diabetes.
The authors noted that there are many similarities between the symptoms associated with Covid-19 and those seen in diseases caused by amyloids. Therefore, they focused on the study of proteins in the envelope of the SARS-CoV-2 virus and the possibility of forming amyloids from them.
The functions of proteins, in addition to the sequence of amino acid monomers, are strongly influenced by their secondary and tertiary structures: that is, how these molecules are folded, their three-dimensional structure.
In addition to its main form, the protein can take on an alternative form, which, most likely, will not perform any function in the cell and will simply accumulate as ballast.
Over 30 different proteins are known to have this alternative form of amyloid, which is usually associated with the development of some disease.
Using computer simulations, the researchers found that the SARS-CoV-2 coronavirus spike protein (S-protein), which it uses to interact with and infect body cells, contains seven sites that can produce amyloid.
Three of the seven sites were able to form not just amyloid, but amyloid fibrils large, branched structures that look like long, tangled filaments when viewed under an electron microscope.
We wanted the best, but it turned out …
However, the potential for the formation of amyloids does not mean anything if there is no mechanism by which they can be formed in the body.
And, probably, the authors found it: the leukocytes of the immune system, trying to protect the body from the virus, secrete an enzyme that cuts the proteins of the virus envelope, destroying it and preventing cell infection.
Unfortunately, in the process, exactly one of those sites that form long amyloid fibrils is formed in large quantities.
“We have never seen fibrils as perfect yet terrifying as those derived from the amyloid-producing SARS-CoV-2 spike protein and its fragments. The fibrils formed from fragments of the spike protein branched out like tentacles. Amyloids don’t usually branch like that.
We think this is due to the characteristics of the protein itself,” explained Per Hammarström , professor in the Department of Physics, Chemistry and Biology at Linköping University and co-author of the study.
Previous work has shown that the SARS-CoV-2 spike protein may be involved in the formation of small blood clots.
Blood contains the protein fibrin, which helps it clot when a vessel is damaged so as to close the hole and stop bleeding. After the wound has begun to heal, the coagulant (the same patch that closes the hole in the vessel) is normally broken down by plasmin, another protein also found in the blood.
Knowing this, the Swedish scientists mixed fragments of the amyloid-producing spike protein with these blood proteins and saw that the resulting coagulate of fibrin and amyloid fibrils was not cleaved by plasmin as usual.
Thus, this mechanism may be responsible for the formation of similar blood microclots that are observed in both severe and long-term Covid-19. Further research, in particular, observation of real patients, is needed to confirm the role of the open mechanism in the formation of severe symptoms of coronavirus infection.
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