SARS-CoV-2 Spike Protein Causes Novel Inflammatory Blood Clotting

This paper has just been published. It's a preprint so hasn't been formally peer-reviewed, and that should be borne in mind when analysing its conclusions.

Here we report that the Spike protein from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the blood coagulation factor fibrinogen and induces structurally abnormal blood clots with heightened proinflammatory activity. SARS-CoV-2 Spike virions enhanced fibrin-mediated microglia activation and induced fibrinogen-dependent lung pathology. COVID-19 patients had fibrin autoantibodies that persisted long after acute infection. Monoclonal antibody 5B8, targeting the cryptic inflammatory fibrin epitope, inhibited thromboinflammation. Our results reveal a procoagulant role for the SARS-CoV-2 Spike and propose fibrin-targeting interventions as a treatment for thromboinflammation in COVID-19.

Persistent life-threatening thrombotic events are a hallmark of COVID-19. Aberrant clots form in multiple organs causing significant morbidity and mortality in COVID-19 patients (1, 2). The high incidence of clotting complications has been attributed to disease severity, inflammation and subsequent hypercoagulable state (3). However, the clinical picture is puzzling because of disproportionate rates of thrombotic events and abnormal clot properties not observed in other inflammatory conditions, such as severe sepsis or different viral respiratory illnesses (4-7).

The central structural component of blood clots, and a key regulator of inflammation in disease, is insoluble fibrin, which is derived from the blood coagulation factor fibrinogen and is deposited in tissues at sites of vascular damage (10, 11). Hypercoagulability in COVID-19 is associated with inflammation and the formation of fibrin clots resistant to degradation despite adequate anticoagulation (3-5).

The high prevalence of thrombotic events with these unique hypercoagulability features suggests an as yet unknown mechanism of abnormal blood clot formation in COVID-19. We set out to determine how blood clots form in COVID-19 and to identify therapies to combat the deleterious effects of abnormal coagulation occurring in acute and convalescent stages of disease. Since hypercoagulability in COVID-19 patients has features distinct from those of other inflammatory diseases, we hypothesized that SARS-CoV-2 directly affects the structural and functional properties of blood clots.

So what we have is a virus which, in a relatively few serious cases, mainly in older people and those with co-morbidities, causes a unique form of pro-inflammatory blood clotting which has not been observed in other respiratory diseases and in fact appears to be a phenomenon new to medicine. It is these structurally abnormal clots which are responsible for many of the fatalities associated with SARS-CoV-2 infection.

What is causing these 'structurally abnormal' blood clots? The authors identify the SARS-CoV-2 spike protein as the culprit, the mechanism which involves the binding of the spike to one of the key ingredients of blood clots, fibrin:

The central structural component of blood clots, and a key regulator of inflammation in disease, is insoluble fibrin, which is derived from the blood coagulation factor fibrinogen and is deposited in tissues at sites of vascular damage (10, 11). Hypercoagulability in COVID-19 is associated with inflammation and the formation of fibrin clots resistant to degradation despite adequate anticoagulation (3-5).

Overall, these results reveal an unanticipated role for SARS-CoV-2 Spike as a fibrinogen binding protein that alone accelerates the formation of abnormal clots with altered structure and increased inflammatory activity.

It's not the virus causing this damage; it's the spike protein alone. The biologically engineered spike protein, in all likelihood. Fauci's biologically engineered spike protein, that is.

The high prevalence of thrombotic events with these unique hypercoagulability features suggests an as yet unknown mechanism of abnormal blood clot formation in COVID-19.

I bet it's not unknown to Fauci and his co-conspirators who designed this virus and, with the help of the CCP, unleashed it upon an unsuspecting world. You think maybe that's a tin foil hat too far? I don't think so. A huge amount of evidence now points to the man-made origin of the SARS-CoV-2 virus and its deliberate or, less likely, unintentional release to create a planned pandemic. You might want to pre-order Robert F. Kennedy Jr.'s book on Fauci and his role in creating this plandemic and corrupting medical science along the way.

Since hypercoagulability in COVID-19 patients has features distinct from those of other inflammatory diseases, we hypothesized that SARS-CoV-2 directly affects the structural and functional properties of blood clots. Incubation of SARS-CoV-2 recombinant trimeric spike protein (Spike) with healthy donor plasma increased fibrin polymerization (Fig. 1A). Spike strikingly altered the fibrin clot structure resulting in thinner fibers with a rough appearance and increased clot density as shown by scanning electron microscopy (SEM) (Fig. 1B, fig. S1),

It's not just spike proteins building abnormal blood clots which is a problem though, it's even worse. The spike-induced fibrin accumulation at bodily sites actually causes more inflammation:

Fibrin is deposited locally at sites of vascular damage and is a potent proinflammatory activator and a key inducer of oxidative stress (11, 18). Strikingly, Spike increased fibrin-induced release of reactive oxygen species (ROS) in a concentration-dependent manner in bone marrow derived macrophages (BMDMs), while Spike alone did not have an effect (Fig. 1G). These results suggest a role for Spike as an enhancer of fibrin-induced inflammation at sites of vascular damage. Overall, these results reveal an unanticipated role for SARS-CoV-2 Spike as a fibrinogen binding protein that alone accelerates the formation of abnormal clots with altered structure and increased inflammatory activity.

If the SARS-CoV-2 full length spike protein architecture is indeed a product of man, not nature, then it is quite obviously designed to be a lethal bioweapon of particularly fiendish effectiveness.

These results reveal a Spike–fibrinogen-dependent mechanism of clot formation that generates strong inflammatory and oxidative stress responses.

Fibrinogen is causally linked to the activation of macrophages and microglia in autoimmune and inflammatory diseases in the brain and periphery (11, 21). Fibrin is a driver of microglia-induced cognitive dysfunction (22) and is associated with perivascular-activated microglia and macrophages in brains of COVID-19 patients even without signs of infection (12).

Nasty. The authors summarise their findings as follows:

In summary, we find that SARS-CoV-2 Spike protein enhances the formation of highly inflammatory clots that are neutralized by a fibrin-targeting monoclonal antibody. Our data shed new light on the enigmatic coagulopathy found in COVID-19 revealing a causal role for fibrinogen in thromboinflammation – even independent of active viral replication. The high incidence of clotting complications in COVID-19 has been attributed to systemic inflammation (3), vascular damage including abnormal levels of circulating coagulation proteins (1, 26), genetic susceptibility to tissue factor and complement genes (27), and prothrombotic autoantibodies (28). Our findings now show that coagulopathy is not merely a consequence of inflammation. Rather, the interaction of SARS-CoV-2 Spike with fibrinogen and fibrin results in abnormal blood clot formation that in turn drives inflammation. Identification of SARS CoV-2 Spike protein as a fibrinogen binding partner provides a mechanistic basis for the formation of abnormal clots with enhanced inflammatory properties.

A vicious circle. Coagulation is not merely a result of inflammation, it causes inflammation also, a process driven by the presence of the spike protein alone and its peculiar interaction with fibrinogen and fibrin.

Now here's the kicker. If the SARS-CoV-2 virus with its uniquely pathogenic spike protein is a bioweapon, then so also must be the 'vaccines', which cause the cells in our bodies to manufacture SARS-CoV-2 spike proteins in their trillions, and it has been demonstrated conclusively that these spikes find their way into the vascular system and circulate to every organ in the body, even the brain. Go figure, as they say.