Postdoctoral Research Associate Kate Marks has been awarded a Visiting Fellowship to Linköping University in Sweden.

Long COVID, or postacute sequelae of COVID-19 from SARS-CoV-2 infection, is a persistent debilitating disease affecting multiple systems and organs. Long COVID pathophysiology is a complex and not fully established process. One prevailing theory is that the formation of fibrin amyloid microclots (fibrinaloids), due to SARS-CoV-2 infection, can induce persistent inflammation and capillary blockage. An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis was made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein mediated resistance to plasmin lysis. Here, we use purified components from the coagulation cascade to investigate the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen–fibrin–fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601–620) impaired thrombin-mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On the contrary, fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685–701) exhibited a marked resistance to plasmin-mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks as well as incorporate fibrin into aggregated structures that resist fibrinolysis. Our study proposes a molecular mechanism for how the Spike protein of SARS-CoV-2 could contribute to the formation of fibrinolysis-resistant microclots observed in long COVID.

The 8th European Conference on Social Networks (EUSN 2026) will take place on 11–15 August 2026 in Norrköping, Sweden, hosted by the Institute for Analytical Sociology (IAS), Linköping University. The...

Vårt Djurgårdslag är tillbaka hemma på Hovet och nyförvärvet Daniel Marmenlind tar klivet in i matchtruppen. Tränarteamet formerar fyra fulla formationer, med Daniel Brodin som extraspelare. Pucken släpps 19:00 framför helt slutsålda läktare - full fart framåt!

SHL-veckan startar med torsdagshockey i huvudstaden och med en ny publikfest i gult, rött och blått. Efter två raka förluster laddar vårt Djurgårdslag för att resa sig när Linköping nu gästar, ett motstånd som tuggat igång efter uppehållet. Sjung fram Djurgår’n från läktarplats och stötta DIF Hockey Ungdom genom 50/50-lotten - vi ses på Hovet!