HomeScientists Have Finally Found A Mechanism Behind Strange Covid-19 Symptoms

Scientists Have Finally Found A Mechanism Behind Strange Covid-19 Symptoms

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A new study suggests that harmful amyloid formation and COVID-19 symptoms may be linked.

People who have had COVID-19 for a long time often have blood coagulation issues. Now, scientists at LiU have found that the body’s immune system can change the SARS-CoV-2 virus’s spike protein, causing the virus to make a misfolded protein called amyloid.

It is possible for organs other than the lungs to be badly impacted in individuals who have severe and long-term COVID-19. Complex symptoms and damage to the heart, kidneys, eyes, nose, and brain, as well as blood coagulation problems, can all persist. It’s unclear why the sickness affects the body in this way. Now, LiU researchers have discovered a previously unknown biological process that could contribute to the answer.

The research team looks into diseases caused by proteins that don’t fold correctly. Alzheimer’s disease in the brain is the best-known example of this. COVID-19-related symptoms share many parallels with those seen in disorders caused by misfolded proteins, according to the researchers.

The fact that proteins are folded in unique ways that give rise to a specific three-dimensional structure has a significant impact on their functions. A protein can take on another shape in addition to this one. Over 30 distinct proteins are known to have this unusual structure, which has been linked to disease. Amyloid is the name for this alternate folded protein. The LiU scientists wondered if the SARS-CoV-2 virus, which produces COVID-19, contains an amyloid-forming protein. They were particularly interested in the spike protein on the virus’s surface, which the virus utilizes to interface with and infect the body’s cells.

Using computer simulations, the researchers found that the spike protein of the coronavirus had seven different sequences that could lead to the formation of amyloid. When tested experimentally, three of the seven sequences met the researchers’ criteria for being classified as amyloid-producing sequences. They created fibrils, which seem like lengthy threads when seen under an electron microscope.

But do these fibrils appear on their own? Many diseases, such as Alzheimer’s, are preceded by a process in which the body breaks down big proteins into tiny fragments, which can lead to the production of toxic amyloid. In their study, which was published in the Journal of the American Chemical Society, the authors have found that an enzyme from the white blood cells of the immune system can cut up the spike protein of the coronavirus. When the spike protein is torn up, it creates the exact fragment of the protein that is most likely to produce amyloid, according to the researchers’ analyses. This enzyme is produced in great quantities by neutrophils, a type of white blood cell that is discharged early in infections like COVID-19. When the researchers combined pure spike protein with the enzyme neutrophil elastase, they got strange fibrils.

“We have never seen such perfect, but scary, fibrils as these ones from the amyloid-producing SARS-CoV-2 spike protein and pieces thereof. The fibrils starting from the full-sized spike protein branched out like limbs on a body,” explains Per Hammarström, a professor at Linköping University’s Department of Physics, Chemistry, and Biology (IFM), “Amyloids don’t usually branch out like that. We believe that it is due to the characteristics of the spike protein.”

Earlier studies, including one research by South African researchers, have revealed that the spike protein may be involved in the development of tiny blood clots. When a vessel is damaged, the fibrin protein in the blood assists the blood to coagulate, sealing the hole and stopping the bleeding. The coagulate is expected to be broken up by plasmin, which is also contained in blood, once the damage has started to heal. The LiU researchers combined amyloid-producing protein fragments from the spike protein with these biological fluids in test tubes and discovered that the fibrin coagulate that resulted could not be broken down by plasmin in the usual way. This newly identified process could be responsible for the formation of identical tiny blood clots seen in both serious and long-term COVID-19 cases. In many amyloid-related disorders, blood coagulation is disrupted.

“We can see that the spike protein, when affected by our own immune system, can produce amyloid structures, and that this can potentially affect our blood coagulation,” adds Sofie Nyström, an associate professor at IFM and the study’s second author. “We believe that this discovery is significant for many fields of research, and we hope that other researchers will examine the questions that it raises.”

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