Johnson & Johnson, Explanations for Clotting ? – Part 4

My annotations in blue.

We’ve looked at how an adenovirus vector, by migration away from the injection site,  could challenge the  immune system in ways not intended by vaccine design. It would not be surprising, since many challenges, even absent infection, such as sterile surgical inflammation, can cause immune system dysregulation.

Dysregulation is a term used a lot in the literature. It occurs when the immune system becomes too active, as with autoimmunity, or is suppressed, as caused by many viruses. It covers a mountain of ignorance. While specific feedback/control mechanisms have been studied in detail,   there is no unified theory of the whole thing. As part of our hypothesis, the adenovirus vector causes dysregulation by liver toxicity.

Once  you get out of comfy Middleton’s Allergy (which old-used is like $20), immune system literature  is like leaving your cozy house out to a blinding blizzard. Facts,  statistics, associations,  implications, and hunches  hit your eyes and crust your glasses, while icicles grow down to your keyboard. Even something as simple as a platelet becomes the research of someone’s lifetime, while someone else spends years trying to fit that work to a broader context.

Clotting disorders are a feature of many virus infections. Have virologists acquired anything useful on why an adenovirus vector would cause a clotting disorder?  (PMC) Thrombocytopenia in Virus Infections, is a meta-study, which winnows 413 PubMed search results into 203 papers that were actually read. Results are presented in tables. HIT is not referenced; PF4 gets a single mention with Zika fever. The sought-after secret, a relation between virus, dysregulation and clotting, is not in plain view.

In high school biology, we learned that platelets are simple plug-the-hole pellets, fragments of other cells, without a nucleus, maybe not even alive. Wrong! Quoting from (PMC) Thrombocytopenia in Virus Infections,

Conversely, platelets also affect the inflammatory response to viral infection and can even internalize [engulf] several viruses [and bacteria] directly. In response to infection, platelets interact with leukocytes [white blood cells] and vascular endothelial cells [lining of blood vessels] before activating and secreting soluble prothrombotic [causing clots] and…

Platelets do some  things similar to the functions of white blood cells, but with differences of style. Their roots are different: the innate and adaptive immune systems. which were formerly thought to be separate. The innate system goes back to the dawn of life;  its logic was thought to be “shoot on sight.”  The adaptive system, thinking as much as something without a brain can, crafts an individual response to each challenge.

The above picture is obsolete; the innate and adaptive systems are highly interdependent. The next steps of our hypothesis:

  • The platelet is a bridge between the innate and adaptive immune systems.
  • Dysregulation of either system results in dysregulation of the other.
  • The  antibodies of HIT (heparin induced thrombosis) are not inherently pathological. They are a normal occurrence, observed in normal individuals. They exist as a necessary part of the bridge between the innate and adaptive systems.
  • HIT antibodies, when amplified by immune dysregulation, are pathological.

Support from literature will be provided. To be continued shortly.

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