Laridae birds, such as gulls, are known reservoirs of H13 and H16 low pathogenic avian influenza subtypes. However, during the recent outbreaks linked to the reemergence of high pathogenicity avian in...

Scientific Reports - Fatigue in children and young people up to 24 months after infection with SARS-CoV-2

Exclusive: Teuta ‘T’ Hoxha has been taken to hospital after 20 days on hunger strike, following the hospitalisation of Kamran Ahmed earlier this week. Harriet Williamson reports.

The Conservative government repeatedly failed to take action to protect disabled people in the early months of the pandemic, even though their risk of dying was twice as high as non-disabled people…

There are moments in history when the creation of a library becomes an act of freedom itself.Here in Gaza, after the genocide, Omar and Ibrahim understood that dreams protected by books do not yield —...

Raju Rage has been a vital educator, vocal campaigner for social … Raisa Kabir needs your support for Help Raju access urgent medical treatment and healthcare

Given the escalating assault on the Palestinians in Gaza and the West Bank, Saturday’s national demo is absolutely crucial. Having agreed the assembly point and route of the march on November 10th, no...

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.

Users are waking up to discover OpenAI leaked their data this morning via a faulty third-party plugin. Here's what you need to know.