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Source: COVID-19 Research  Sep 21, 2021  2 years, 6 months, 3 weeks, 5 days, 23 hours, 10 minutes ago

German Study Finds That SARS-CoV-2 Triggers Never Seen Before Altered Fibrin Clot Structures That Contributes To Thrombosis Risk In Severe COVID-19!

German Study Finds That SARS-CoV-2 Triggers Never Seen Before Altered Fibrin Clot Structures That Contributes To Thrombosis Risk In Severe COVID-19!
Source: COVID-19 Research  Sep 21, 2021  2 years, 6 months, 3 weeks, 5 days, 23 hours, 10 minutes ago
COVID-19 Research: A new study led by German researchers from the Center for Infection and Genomics of the Lung (CIGL), Universities of Giessen and Marburg Lung Center, Giessen-Germany along with scientist from numerous other German research institutions have shockingly found that the SARS-CoV-2 induces the formation of unique and different and fibrin clot structures never seen before in the human body and it is these altered fibrin clot structures that are contributing to thrombosis risk in severe COVID-19 patients.

 
According to the study abstract, “The high incidence of thrombotic events suggests a possible role of the contact system pathway in COVID-19 pathology.”
 
The study team demonstrated altered levels of factor XII (FXII) and its activation products in two independent cohorts of critically ill COVID-19 patients in comparison to patients suffering from severe acute respiratory distress syndrome due to influenza virus (ARDS-influenza).
 
The study team found rapid consumption of FXII in COVID-19, but not in ARDS-influenza, plasma.
 
Interestingly, the kaolin clotting time was not prolonged in COVID-19 as compared to ARDS-influenza.
 
Utilizing confocal and electron microscopy, the study team showed that increased FXII activation rate, in conjunction with elevated fibrinogen levels, triggers formation of fibrinolysis-resistant, compact clots with thin fibers and small pores in COVID-19.
 
The study team also observed clot lysis in 30% of COVID-19 patients and 84% of ARDS-influenza subjects. Analysis of lung tissue sections revealed wide-spread extra- and intra-vascular compact fibrin deposits in COVID-19.
 
The study findings indicate that elevated fibrinogen levels and increased FXII activation rate promote thrombosis and thrombolysis resistance via enhanced thrombus formation and stability in COVID-19.
 
The study findings were published on a preprint server and are currently being peer reviewed. https://www.biorxiv.org/content/10.1101/2021.09.17.460777v1
 
The SARS-CoV-2 coronavirus causes the COVID-19 disease, which is a multisystem disease affecting the respiratory tract. Data available so far shows endothelial injury caused by hyperactivation of the immune system as a major underlying molecular mechanism for COVID-19 severity and mortality. In addition, this endothelial involvement leads to many hemostasis abnormalities in severe COVID-19 patients.
 
Besides elevated levels of pro- and anti-inflammatory mediators such as int