New data from Europe suggest Sweden's laissez-faire approach to the pandemic was far from catastrophic.
For me it is the neurologically damaged that concerns meyeah, same here. apparently the virus itself does not attack nerve tissue (although there are some wild claims that it makes prions) ... the damage is from the inflammatory aftereffects of the virus. but it is damage, just the same. there have been reports all along about losing taste and smell, a very disturbing neurological symptom, along with fatigue and 'brain fog'... in addition to the thromboses.
Here we study the effect of isolated SARS-CoV-2 spike protein S1 subunit as potential pro-inflammatory inflammagen sui generis. We investigate the potential of this inflammagen to directly interact with platelets and fibrin(ogen) to cause fibrin(ogen) protein changes and blood hypercoagulation. We also determine if the spike protein may interfere with blood flow, by comparing naïve healthy PPP samples, with and without added spike protein, to PPP samples from COVID-19 positive patients (before treatment). We conclude that the spike protein may have pathological effects directly, without being taken up by cells.neither KD nor I are virologists, so decide for yourself...
Receptor binding is certainly responsible for cell-mediated pathologies, but does not of itself explain the coagulopathies. Spike protein, can however be shed, and it has been detected in various organs, including the urinary tract (George et al., 2021). S1 proteins can also cross the blood-brain-barrier (Rhea et al., 2021). Free S1 particles may also play a role in the pathogenesis of the disease (Letarov et al., 2020, Buzhdygan et al., 2020). Free spike protein can potentially be released due to spontaneous “firing” of the S protein trimers on the surface of virions, and infected cells liberates free receptor binding domain-containing S1 particles (Letarov et al., 2020).-- and the people who wrote the paper are real scientists.