https://www.mdpi.com/2076-393X/9/1/36/htm
It is generally thought that the sole function of viral membrane fusion proteins is to allow the viruses to bind to the host cells for the purpose of viral entry into the cells, so that the genetic materials can be released and the viral replication and amplification can take place.
However, recent observations suggest that the SARS-CoV-2 spike protein can by itself trigger cell signaling that can lead to various biological processes. It is reasonable to assume that such events, in some cases, result in the pathogenesis of certain diseases.
Our laboratory only tested the effects of the SARS-CoV-2 spike protein in lung vascular cells and those implicated in the development of PAH. However, this protein may also affect the cells of systemic and coronary vasculatures, eliciting other cardiovascular diseases such as coronary artery disease, systemic hypertension, and stroke. In addition to cardiovascular cells, other cells that express ACE2 have the potential to be affected by the SARS-CoV-2 spike protein, which may cause adverse pathological events.
Thus, it is important to consider the possibility that the SARS-CoV-2 spike protein produced by the new COVID-19 vaccines triggers cell signaling events that promote PAH, other cardiovascular complications, and/or complications in other tissues/organs in certain individuals (Figure 3). We will need to monitor carefully the long-term consequences of COVID-19 vaccines that introduce the spike protein into the human body.
Furthermore, while human data on the possible long-term consequences of spike protein-based COVID-19 vaccines will not be available soon, it is imperative that appropriate experimental animal models are employed as soon as possible to ensure that the SARS-CoV-2 spike protein does not elicit any signs of the pathogenesis of PAH or any other chronic pathological conditions.
I didn’t have time to read your link, Cathi, so pardon my impertinence.
Is this saying that any interaction with the ACE2 binding site, triggers the innards of the cell to begin other processes, even when the furin cleavage site is not involved (i.e., the virus never even *enters* the cell) ?
If so, this would go a LONG way towards teasing out a putative mechanism for adverse events subsequent to injection with the mRNA.
In particular, the body is not static; a paper out of Harvard I posted a snippet or link from yesterday, pointed out that the body downregulates ACE2 receptors in the uterus during pregnancy, which happily helps protect the growing baby from COVID during early pregnancy.
But if there is such a thing as downregulation, then there may be upregulation. More ACE2 receptors...I vaguely remember papers from before the c00f left China, showing that Chinese males (I think especially smokers) had many more ACE2 binding sites in their lungs than other groups.
Thanks for posting this.