An overload of inflammatory molecules trapped inside microscopic blood clots could be behind long COVID, according to a Stellenbosch University study in Bioscience Reports.
Prof Resia Pretorius, head of physiological sciences, told the Sunday Times that the study, used plasma samples from healthy individuals, those with type 2 diabetes, acute COVID and long COVID.
“Acute COVID-19 is not only a lung disease, but actually significantly affects the blood flow and blood clotting systems,” Pretorius .
“Our study showed there is significant microclot formation in the blood of both acute COVID-19 and long COVID patients. With healthy physiology, clots may form, for instance, when you cut yourself. However, the body breaks down the clots efficiently by a process called fibrinolysis. In blood from patients with long COVID, persistent microclots are resistant to the body’s own fibrinolytic processes. We found high levels of various inflammatory molecules trapped in the persistent microclots.”
The microclots and hyperactivated platelets, also involved in clotting, result in cells not getting enough oxygen to sustain bodily functions, a condition called cellular hypoxia.
“Widespread hypoxia may be central to the numerous reported debilitating symptoms,” said Pretorius.
Health professionals’ primary focus had been caring for acute COVID patients in hospitals. “Very little attention is given to the severely ill and sometimes disabled people who just never recover from persistent symptoms.”
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19
Lize Grobbelaar, Chantelle Venter, Mare Vlok, Malebogo Ngoepe, Gert Jacobus Laubscher, Petrus Johannes Lourens, Janami Steenkamp, Douglas Kell, Etheresia Pretorius.
Published in BioScience Reports on 20 August 2021
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, the cause of coronavirus disease 2019 (COVID-19), is characterized by unprecedented clinical pathologies. One of the most important pathologies, is hypercoagulation and microclots in the lungs of patients. Here we study the effect of isolated SARS-CoV-2 spike protein S1 subunit as potential inflammagen sui generis. Using scanning electron and fluorescence microscopy as well as mass spectrometry, we investigate the potential of this inflammagen to interact with platelets and fibrin(ogen) directly to cause blood hypercoagulation. Using platelet-poor plasma (PPP), we show that spike protein may interfere with blood flow. Mass spectrometry also showed that when spike protein S1 is added to healthy PPP, it results in structural changes to β and γ fibrin(ogen), complement 3, and prothrombin.
These proteins were substantially resistant to trypsinisation, in the presence of spike protein S1. Here we suggest that, in part, the presence of spike protein in circulation may contribute to the hypercoagulation in COVID-19 positive patients and may cause substantial impairment of fibrinolysis. Such lytic impairment may result in the persistent large microclots we have noted here and previously in plasma samples of COVID-19 patients. This observation may have important clinical relevance in the treatment of hypercoagulability in COVID-19 patients.
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