Pts with severe COVID show complement (C3a)-driven proliferation of pathogenic CD16+ expressing Tcells (CD4+ & CD8+) increase immune complex-mediated, Tcell receptor(TCR)-independent cytotoxicity causing activation/release of chemokines & lung injury.
medrxiv.org/content/10.110…
First demonstration of disease-promoting activity of the complement pathway in COVID (has been shown for other coronaviruses) even w mild disease. This pathway may exacerbate disease via dysfunctional T cell response that causes the localized cytotoxicity and tissue damage.
So the question is, what triggers this disease promoting complement-activation pathway? Spike antigen? Whether the activated CD16 expressing CD4+ and CD8+ T cells are SARS-CoV-2 antigen specific remains unclear.
We do know the spike protein itself (independent of the virus) is capable of altering gene expression likely through altered cell signaling. Perhaps the spike protein itself triggers complement activation? humm? Do you think? Oops
pubmed.ncbi.nlm.nih.gov/32877502/
Now, in people who have just recovered from COVID disease who likely have high organ levels of these dysfunctional Tcells, what do you think happens when you inject them w a plasmid encoding the viral spike protein? Oops.
newjersey.news12.com/new-jersey-man…
Cytotoxicity. Cardiotoxicity. Oh, I dunno. Trust the experts!
Lookie here, ADE comes in all different flavors. C, E (lysis & apoptosis) seem particularly relevant to this discussion. Where spike-producing cells may cause localized inflammation and tissue injury? Wherever there are Abs and complement complexes and spike producing cells?
And one other noteworthy tidbit worth ruminating on
A single sugar makes all the difference
science.sciencemag.org/content/371/65…
Afucosylated IgG are found in alloimmune responses (pregnancy-associated autoimmune attacks of RBC/platelets), HIV, dengue and now SARSCoV2 which are all directed against surface-exposed, membrane-embedded proteins. Is the vaccine-induced spike antigen membrane embedded? Oopsies.
Has anyone bothered to look at the fuglycosylation level of IgG antibodies induced by current mRNA and DNA vaccines and compared that to, ohhh let's say, that seen w the recombinant non-membrane bound protein subunit vaccines?
I have a hunch the VITT, myocarditis we're seeing w membrane-associated spike vaccines have something to do with localized complement-driven Tcell driven cytotoxicity even in ppl without a prior history of COVID exposure. Before the Twatter police censor me, I'd like to say:

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More from @Undergroundsar3

12 Jun
This is an interesting study from the standpoint of understanding and comparing natural immunity to SARSCoV2 vs. vaccines. This paper shows that convalescent serum contains non-neutralizing IgG to S and N protein which helps resolve disease biorxiv.org/content/10.110…
They show IgG Fc-dependent cellular activity triggered via N and S protein antibodies (i.e. antibody dependent phagocytosis and cellular toxicity). ImageImage
If indeed some of the antibodies produced by the virus are pathogenic and activated Tcell responses are pathogenic then rapid clearance of the stimulatory virus particles and dampening of the Tcell immune response would be critical for reestablishing homeostasis.
Read 6 tweets
12 Jun
Ruh roh! Platelets express CD40; might CD40 ligand (CD40L)-positive T cells bind platelets, cause their activation, and trigger granular RANTES release, creating a T cell recruitment feedback loop ?
RANTES quickly binds endothelial surfaces and promptly induces localized leukocyte/DC recruitment and retention. Considering their number and their ability to swiftly release massive amounts of RANTES, these activated platelets may mediate systemic clotting/DIC w vaccines
To my lovely vaxx fetishist follower who censors me at every turn: Image
Read 4 tweets
12 Jun
Evidence that B.1.1.7 (UK) and B.1.351 (SA) SARS-CoV-2 variants display enhanced Spike-mediated fusion due to larger and more numerous syncytia to evade humoral immunity. They remain sensitive to innate immunity components biorxiv.org/content/10.110…
What's particularly curious about this paper is that they generated their own spike vaccines/plasmids and transfected cells to examine the effects of the mutant spikes on cell-cell fusion in vitro in the absence of any other viral protein.
They demonstrate that B.1.1.7 and B.1.351 variants are more potent fusogens than the wild type and DtoG mutations. Expression of these spikes induce more syncytia, but S protein-mediate fusion inhibited by interferon
induced transmembrane proteins (IFITMs).
Read 5 tweets
9 Jun
The cytoplasmic domain of the envelope protein of SARSCoV2 has a DLLV motif that recognizes domains on the gap junction protein, PALS1, and causes it to relocate from cell surface to an intermediate recycling compartment
nature.com/articles/s4146…
The idea is that the cytoplasmic domain of this gap junction protein binds the E protein and then gets hung up in an intracellular compartment rather than serving to form gap junctions at/near the cell surface and providing structural integrity to the epithelial layer
The interesting thing, to my mind, about the E protein di-leucine motif is that it looks very similar to motifs (SSEGVPDLLV) involved in intracellular trafficking of transmembrane proteins to lysosomes and specialized intracelluar compartments
Read 5 tweets
29 May
Evidence that the enhanced transmissibility/pathogenicity of B.1.617 may be due to P681R mutation within the furin cleavage site enabling more efficient cleavage of a peptide mimetic of the B.1.617 S1/S2 cleavage site by recombinant furin. biorxiv.org/content/10.110…
This is one piece of data, to my mind, that doesn't really fit w the lab hypothesis. SARSCoV2 has a furin cleavage site (PRRAR) in its spike protein that is absent in other group-2B coronaviruses. This current study and prior studies have shown the furin cleavage site...
Is a key feature in replication and pathogenesis. Why would someone intentionally engineer a proline in the PRRAR site when clearly one would anticipate the bulky proline to hinder furin function?
Read 7 tweets
29 May
Ok, this is disturbing. Biodistribution studies should have been done BEFORE Phase 3 testing. Detection of vaccine vector copies were found in all mouse tissues analyzed; evidence of imminent vector spread into the blood stream and different organ tissues biorxiv.org/content/10.110…
Sure would like to know the AEs patient #4 and #7 had over the course of a week post-vaccination. Would be nice to correlate safety/tolerability with this persistence of vector DNA in the plasma, huh?
Read 4 tweets

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