Thread by @FizeekBio

I develop fixations in my studies. I develop fixations on elements that present promise in connecting dots. It's all one big puzzle, and my goal is to make the pieces fit. I can't do it without developing these fixations.

#SARSCoV2, microclots, infarcts, multi-organ damage.

#SARSCoV2 inhibits Type-1 interferon (IFN). This is its evolutionary advantage over its predecessor SARSCoV, & likely the reason behind the asymptomatic phenomenon, since IFN ➡️ immune activation, inflammation, fever ➡️ symptoms.

This is what makes #COVID19 special.

We also know that IFN is critical in facilitating a switch from innate immunity (nonspecific defenses like neutrophil NETosis & platelet-induced coagulation) to adaptive immunity (highly specific defenses involving T/B cells & antibody production).

If Type-1 IFN is inhibited, how much does that inhibit, or delay, adaptive immunity (T cell, B cell activation, antibodies)? How much does that then skew the share of the battle back onto primitive defenses like innate immunity + complement (➡️⬆️ immunothrombosis/microclotting)?

The over-reliance on immunothrombosis/microclotting during an acute #COVID19 infection is evident and well-documented.

This likely explains why #SARSCoV2 induces 9x more microclots than #influenza.

The outcome of pervasive microclotting, visualized;

Microvascular thrombosis in 85% of patients with severe #COVID19, w/ 31% exhibiting completely stagnated capillaries. Small sample size in this study of sublingual tissue.

Pervasive microclotting has consequences for organs across the body because it disrupts blood-flow dynamics, and thereby risks oxygen-deprivation-related damage.

The consequences therein on the brain intrigue me most of all.