Dysregulated blood coagulation is frequently reported in people with long-term COVID-19. SARS-CoV-2 viral spike proteins may be affected by the innate immune system, according to new study from Sweden’s Linköping University (LiU). This can contribute to amyloid, a misfolded spike protein, forming on the exterior of the virus.
Tissues besides the lungs may be seriously damaged in persons with significant and long-term COVID-19. Signs and injury to several organs, including the heart, the kidneys & eyes, the nose, and the brain, and also problems with blood coagulation, may occasionally persist. The illness’s exact mechanism of action on the body has remained a mystery for the most part. Scientists at LiU have discovered a previously unknown biochemical pathway that may help explain the phenomenon.
Denatured proteins, such as Alzheimer’s illness in the brains, are the focus of the study team’s efforts. COVID-19-related symptoms have a lot in common with those seen in disorders caused by misfolded proteins, according to the researchers.
There are around 30 distinct proteins that exhibit this kind of disease-associated alternate form. It’s called amyloid because of the way it’s folded. COVID-19 is caused by the virus SARS-CoV-2, which may include an amyloid-producing protein, according to LiU scientists. It was the spiking protein on the virus’ exterior, which the virus utilizes to attack cells, that they were most interested in.
The spike protein has been linked to the formation of tiny blood clots in earlier studies, along with a research by South African experts. When a blood artery is injured, the fibrin protein in the bloodstream assists the blood clot so that the hole closes and the hemorrhage ceases. In theory, plasmin, another protein present in blood, would break apart the coagulate as the wound heals.
Tiny clots that have been shown in both severe and long-term COVID-19 may be caused by this newly found process. Many amyloid-related disorders are accompanied by abnormalities in clot formation.