Perico et al. in CELL: "SARS-CoV-2 and the spike protein in endotheliopathy"; this paper helps further clarify that COVID (severe) is less of a respiratory illness & is a blood clotting (thrombosis)

illness; argument is that we can infer strongly that spike protein vaccine induced causes extensive cardiovascular (endothelial) damage; vascular dysfunction & thrombosis is most severe complication

https://www.cell.com/action/showPdf?pii=S0966-842X%2823%2900189-0

SARS-CoV-2, the causative agent of COVID-19, primarily affects the epithelial compartment in the upper and lower airways.

There is evidence that the microvasculature in both the pulmonary and extrapulmonary systems is a major target of SARS-CoV-2. Consistent with this, vascular dysfunction and thrombosis are the most severe complications in COVID-19.

The proinflammatory milieu triggered by the hyperactivation of the immune system by SARS-CoV-2 has been suggested to be the main trigger for endothelial dysfunction during COVID-19. More recently, a rapidly growing number of reports have indicated that SARSCoV-2 can interact directly with endothelial cells through the spike protein, leading to multiple instances of endothelial dysfunction. Here, we describe all the available findings showing the direct effect of the SARS-CoV-2 spike protein on endothelial cells and offer mechanistic insights into the molecular basis of vascular dysfunction in severe COVID-19.’

Among the distinctive features of severe COVID-19, endothelial cell injury and dysfunction – also termed ‘endotheliopathy’ – have been identified as the most frequently reported complications that correlate with disease mortality [1,2]. The initial observation of endothelial dysfunction following SARS-CoV-2 infection was gained primarily from autopsy studies, which showed widespread thrombosis with microangiopathy in alveolar capillaries in COVID-19 patients that were nine times more frequent than in patients with influenza [3].

In lung autopsies from COVID-19 patients, virus dependent endothelial cell injury was found to be associated with infiltration of inflammatory cells into perivascular tissues [3]. The higher incidence of vascular injury and thrombosis in the lungs of patients who succumbed to SARS-CoV-2 [4] has been postulated to be the underlying cause of the ventilation-perfusion mismatch and impaired oxygen uptake that characterize the respiratory complications of severe COVID-19 pneumonia [5].’

This is why McCullough, myself, others have been discussing the blood thinning properties of NATTOKINASE etc. with its blood thinning properties given the risk due to blood clots especially in microcapillaries.

Link to examine the Spike dissolving Recovery formulation:

https://www.twc.health/collections/covid19/products/long-haul-formula?ref=Paul

Link to examine the Spike Recovery formulation:

https://www.twc.health/collections/covid19/products/long-haul-formula?ref=Paul