Thread by @FizeekBio

The immune-response and #COVID19. The "Wack-a-Mole" theory.

This is going to be heavy, and technical at points. But it's important that I regurgitate my thoughts. This is my Eureka moment. #SARS_CoV_2

#COVID degrades the epithelial cells of the lungs, and begins infiltrating therein via the epithelial cells of the underlying vasculature.

The immune system reacts by tipping the balance towards clotting (releasing factors that make the blood more “sticky” and conducive to clotting), in effort to stall the intruders right in their point of entry before entering the wider circulatory system.

Neutrophils play a tremendous role therein, and exude "web-like structures" in the bloodstream to catch the virus particles and prevent widespread invasion

The immune system essentially is playing “wack-a-mole” with the virus, and the cytokine storm is a logical response as the virus continues in persistent manner to attack. Virus breaches the endothelium, and the immune system rushes to clot the gap & prevent further invasion.

The evidence of #COVID's resultant impact on the cardiovascular system is clear by now. Even insidious skin-rashes may be an indication of superficial clotting close to the skin.

One Germany study even MRI-imaged the hearts of previously infected patients 2-3 months after their illness subsided, and noted that 78% (!!) displayed heart abnormalities, and 60% (!!!) displayed ongoing myocarditis (inflammation of the heart muscle).

Knowing all of this, what triggers my unrelenting curiosity is why the fever is not initiated earlier. The fever is a primitive strategy to scorched-earth viruses/pathogens. The very critical role fevers play in the immune response are lightly summarized in these excerpts.

And yet, we know a great majority of those infected will never develop a fever. This includes some who will go on to unfortunately pass away.

Also intriguing is that, even those who do develop fever, often only ever reach a “low-grade fever.” This virus is ostensibly battling the desire of the body to induce fever, and thereby results in merely a low-grade fever that is remarkably restrained in effect

So what causes #SARS_CoV_2 patients to exhibit resistance to fever-induction?

The answer may lie in its encoded genes.

"SARS-CoV-2 ORF3b Is a Potent IFN-I Antagonist"

What's IFN-1?

It plays a tremendous role in the immune-response to pathogens. One such role is its pyrogenic potential;

Eureka.

#SARS_CoV_2 --| [ IFN-1 -> fever ]

Translated: COVID could potentially inhibit the body's ability to induce fever by inhibiting the type-1 interferon.

Inhibited interferon type-1 imparts on the infection an extended length of stay in the body, and thereby increases its potential for systemic infiltration, and its contagiousness (longer duration of illness, absence of fever/symptoms, greater potential for spread).

Absent a fever, we have a scenario whereby the immune system begins playing "#wack_a_mole" with the virus, using neutrophil webs and "sticky-blood" (blood conducive 2 clotting) to patch points of entry into the wider circulatory system.

Perhaps this is COVID's right to success.

RT, share, comment. I posted this for discussion, for food-for-thought. Antagonistic views, views in complement; all are welcome. I ultimately am fixated on learning more, and I can only do that with your help.

& Good luck 2 everyone as we weather the pandemic's second wave.