We continue from Johnson & Johnson, Explanations for Clotting ? – Part 2, where the liver is described as a kind of jail for viruses. It is also an EPA Superfund site, where many of the features of the blood-borne immune response are replicated as stationary recycling operations. In goes a shiny virus with a blown motor; out comes scrap metal. This operation looks like a typical by-the-side-of-the-railroad-tracks recycler. Awaiting their fate, pathogens are stuck to walls with glue, or stored inside cells, sorted in special sacks, called endosomes.
The liver does all this while metabolizing myriad small-molecule poisons, such as the ethanol in the fine Chablis you just had.
Adenoviruses are natively toxic to the liver, just by being themselves. But what about the inner genome, which is activated when a virus successfully enters a cell? A competent virus hijacks a cell to make more of itself, frequently destroying the cell. An adenovirus vector does not have the ability to reproduce. It still frequently destroys the transfected cell, which in measured degree is thought to be a good thing.
It might not be such a good thing if the transfected cell is in the liver. Nota bene: While specific features of the immune system are understood in great detail, the overall regulation of immune response remains a mystery. The most viable theory has a huge hole. In place of this, piecemeal ideas fill the gap. The immune system responds more reliably to a possible pathogen if there is also some damage, indicated by the signals of a dying cell.
Spike protein has been found to be toxic, even when not formed into a complete spike:
- (BioRXiv) An insight into neurotoxic and toxicity of spike fragments SARS-CoV-2 by exposure environment: A threat to aquatic health?
- (Nature) The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice.
- (ScienceDirect) The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood–brain barrier.
Quoting from the last,
Evidence provided suggests that the SARS-CoV-2 spike proteins trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.
From the sum of three papers, a suspicion arises that might otherwise be dismissed: Even short peptide sub units of spike protein may cause harm if sufficient quantities end up in the wrong places.
The quantity of spike protein that ends up in the wrong place depends on mobility (how well it travels). There is a crucial difference between traditional vaccines that contain antigen, and the new technologies: mRNA, and adenovirus-vector, which cause cells of the recipient to make antigen.
A vaccine which contains antigen usually contains an adjuvant substance. How adjuvants improve vaccines is frequently revised, but there is one constant. Whether an adjuvant consists of microscopic oily droplets of squalene, or tiny crystals of alum, it binds the small antigen molecule to a much larger one. This reduces the mobility of the antigen, so it sticks near the injection site.
- When the spike antigen produced by a new vaccine leaves the cell, it is bound to nothing larger. Compared to spike protein bound to adjuvant, it can travel fast and far.
- This is mitigated with mRNA vaccines by the fragility of mRNA, so the producing cells remain clustered.
- This is exacerbated by adenovirus vectors, which are stable.
To be continued.