Further Thoughts On Those Fibrous Vascular Clots

So, I wrote this yesterday:

So there’s your pro-inflammatory positive feedback loop explained in a scientific study published in October 2021 and there is your direct link between pulmonary fibrosis, huge white rubbery ‘blood’ clots and the presence of SARS-CoV-2 genetically engineered and patented spike protein, either by infection with SC-2 virus or by injection with the Covid gene-based ‘vaccines’. The fact that the white rubbery blood clots were not being observed prior to the mass vaccination campaign suggests very strongly that the spike activation of CD147 and the triggering of the TGF-β pathway is much more dangerous in vaccinated people who have trillions of these spikes in their blood stream and organs, which have been modified to be more resistant to degradation than the viral spike.

But then I thought about it and thought, for this to be true, CD147 would have to be facilitating SC-2 spike binding to endothelial cells, not just lung cells. The first requirement for that to happen is that CD147 is expressed on the surface of endothelial cells. It is:

CD147, a transmembrane glycoprotein, is expressed on all leukocytes, platelets, and endothelial cells.

But there’s some disagreement about the relative importance of CD147 binding and ACE2, the latter of which was thought in the early months following the appearance of Covid-19, to be the primary receptor via which the virus infected host cells. In fact, one study, published January 2021 even suggested that CD147 played no role at all in receptor binding:

The spike protein of SARS-CoV-2 is known to enable viral invasion into human cells through direct binding to host receptors including ACE2. An alternate entry receptor for the virus was recently proposed to be basigin/CD147. These early studies have already prompted a clinical trial and multiple published hypotheses speculating on the role of this host receptor in viral infection and pathogenesis. Here, we report that we are unable to find evidence supporting the role of basigin as a putative spike binding receptor. Recombinant forms of the SARS-CoV-2 spike do not interact with basigin expressed on the surface of human cells, and by using specialized assays tailored to detect receptor interactions as weak or weaker than the proposed basigin-spike binding, we report no evidence for a direct interaction between the viral spike protein to either of the two common isoforms of basigin. Finally, removing basigin from the surface of human lung epithelial cells by CRISPR/Cas9 results in no change in their susceptibility to SARS-CoV-2 infection.

But a consensus has since emerged that both CD147 and ACE2 do play a significant role in viral entry into host cells. Here for instance, from June 2022:

Recently, Wang et al. and others have examined the potential role of CD147 as an entry site for SARS-CoV-2 [25]. They demonstrated that CD147 had a higher value of expression in Vero E6 cells in comparison to ACE2. They also observed that CD147 can bind to the RBD region of viral spike protein with high affinity.

In particular, a recent study found that kidney cells were infected primarily via CD147:

Rather than ACE-2 receptors, Kalejaiye et al. found that binding to CD147 receptors on stem cell-derived kidney podocytes is the preferred mechanism through which SARS-CoV-2 infects these cells.

So, we’ve established that endothelial cells do have CD147 receptors on their surface and that, in some cases at least, CD147 plays a significant or even primary role in host cell receptor binding to the viral spike protein. So, we then ask ourselves, does CD147 play a significant, or even dominant role in the binding of the spike to endothelial cells? Remarkably, a study published two and a half years ago, may provide the answer to that question:

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is associated with a wide range of systemic manifestations. Several observations support a role for vascular endothelial dysfunction in the pathogenesis including an increased incidence of thrombotic events and coagulopathy and the presence of vascular risk factors as an independent predictor of poor prognosis. It has recently been reported that endothelitis is associated with viral inclusion bodies suggesting a direct role for SARS-CoV-2 in the pathogenesis. The ACE2 receptor has been shown to mediate SARS-CoV-2 uptake and it has been proposed that CD147 (BSG) can function as an alternative cell surface receptor. To define the endothelial cell populations that are susceptible to infection with SARS-CoV-2, we investigated the expression of ACE2 as well as other genes implicated in the cellular entry of SARS-Cov-2 in the vascular endothelium through the analysis of single cell sequencing data derived from multiple human tissues (skin, liver, kidney, lung and intestine). We found that CD147 (BSG) but not ACE2 is detectable in vascular endothelial cells within single cell sequencing datasets derived from multiple tissues in healthy individuals. This implies that either ACE2 is not expressed in healthy tissue but is instead induced in response to SARS-Cov2 or that SARS-Cov2 enters endothelial cells via an alternative receptor such as CD147.

Note: ‘healthy individuals’. This implies that up until the time of vaccination, healthy individuals do not express ACE2 in endothelial cells, but their endothelial cells do express CD147. So when those spikes start rushing through their veins and arteries, the only way they can bind to endothelial cells is via CD147, thus confirming that CD147 spike binding and the triggering of the TGF-β pathway happens inside the veins and arteries of (previously healthy) Covid-19 vaccinated individuals, as well as the lung tissue (where it results in pulmonary fibrosis). Et voila, the ‘Died Suddenly’ horrific post mortem fibrous clots.