Spike protein hijacks our cells' natural shields

Thrombosis, organ damage, and hyper-inflammation explained (again)

I have discussed SARS-CoV-2 spike protein’s ability to bind heparin back in July, 2022 but not in the context of factor H (FH) protein. Yesterday I wrote an article about the mechanism of action of protection that our cells use to protect themselves from complement-mediated destruction, which incidentally, is “borrowed” by the bacteria Neisseria menigitidis.

Heparin is a highly sulfated variant of heparan sulfate. All that means is that these two molecules are structurally related and differ primarily in their cellular origin, sulfation levels, and biological functions.¹

Figure 1: Heparin and heparan sulfate. https://www.creative-biolabs.com/anti-glycan-antibodies/heparan-sulfate-heparin-structural-differences-biological-roles.htm.

But, does spike bind both? Yes, it does. This has staggering implications that go far beyond messing up the coagulation cascade.

Let me explain.

The literature indicates that SARS-CoV-2 spike binds heparan sulfate via specific residues, especially in the RBD, with length- and sequence-dependent affinity, influencing viral entry and infection.²³⁴⁵ What does this have to do with FH - the key negative regulator of the alternative complement pathway?

Well, since spike protein interacts with cell-surface heparan sulfate (HS), it can interfere with the normal regulatory function of FH by competing for binding sites for FH thus contribute to excessive complement activation, and this is precisely what has been reported in the literature and observed in pharmacovigilance databases as well.⁶⁷⁸

If you have a peek at VAERS and query complement-mediated destruction by pulling out reports with search_terms <- c(”complement”, “factor h”, “factor-h”, “factorh”, “c3”, “c5b-9”, “membrane attack complex”, “thrombotic microangiopathy”, “atypical hemolytic uremic”, “hemolytic uremic”, “complement mediated”, “complement activation”) as keywords within MedDRA codes, you get the following plot by year:

Figure 2: VAERS reports related to complement-mediated/FH involvement from 2019-2025.

This bar chart shows the absolute number of reports involving complement or FH-related AEs and it’s clear that something anomalous happened in 2021.

The rates per 100,000 total reports per year show the same picture in that something happened in 2021 and it is NOT due to more shots being administered.

Figure 3: VAERS reports related to endothelial damage from 2019-2025.

VAERS is definitely throwing a red flag here.

The possible mechanism of action resulting in these anomalistic reporting rates for complement and FH-related AEs in VAERS involves spike protein competing with FH for heparan sulfate binding sites as shown below in Figure 4.

Figure 4: Left - Normal State: Factor H binds the heparan sulfate chain (via its SCR7 and SCR20 domains), keeping complement activation under control through C3b inactivation. Right - SARS-CoV-2 Infection: The spike RBD occupies the same HS binding site using its positively charged residues (Arg346, Arg355, Lys444, Arg466, Arg509), electrostatically displacing Factor H.

The result of this “move-on-over” displacement of FH for spike is uncontrolled complement activation, inflammation, and tissue damage. This plausible mechanism of action of complement-mediated cell destruction by spike binding offers yet another way that spike protein is entirely destructive to human physiology. Any cell that utilizes the FH protein to avoid complement-mediated destruction can be affected by this mechanism. [6]⁹¹⁰

To contextualize this with numbers, the adult human body contains approximately 30–40 trillion cells (3-4×10¹³) and FH protects the vast majority of these cells from inappropriate or excessive activation of the alternative complement pathway. So if the spike burden is excessively high which would be the case with repeated injections with spike-coding material, all cells would be at risk of effect from this mechanism.

Since FH circulates in plasma (the clear/amber-colored part of blood that has a lot of proteins in it) and binds to host cell surfaces via recognition of polyanionic markers (a polyanion is a molecule or chemical complex having negative charges at several sites¹¹), including heparan sulfate and sialic acid. This binding enables FH to accelerate the decay of the C3 convertase and act as a cofactor for Factor I-mediated inactivation of C3b, thereby preventing uncontrolled amplification of the alternative pathway on healthy host tissues.¹²

In the context spike, which we know can compete with FH for binding sites on cell-surface heparan sulfate, a high systemic spike burden could interfere with this protective mechanism across many tissues. Such elevated and prolonged spike exposure is particularly relevant in the context of the COVID-19 shots since the public were told to keep getting injected with them. And as we all know, spike protein and its encoding material has been shown to persist/be detectable for weeks to months - and in rare case reports, even longer - in circulation or specific tissues.¹³¹⁴

Therefore, if spike levels do become sufficiently high and widespread, a larger proportion of the body’s cells could be placed at increased risk of localized complement dysregulation, potentially contributing to endothelial damage, inflammation, or other complement-mediated effects.

Let’s do endothelial damage¹⁵ for VAERS. Just as a reminder, endothelial cells are really, really important to keep healthy because they line the interior surfaces of our blood vessels and lymphatic vessels and are effectively the gatekeepers of vascular integrity, fluid balance, and inflammation control.¹⁶

Now again, this is circumstantial evidence, but these data are plots of reports from VAERS which, once again, is a pharmacovigilance data system designed to throw safety signals in the context of vaccines and injectables for follow-up investigation.

My hypothesis is much more than that since this mechanism of damage is confirmed in the literature.

How was it possible that they got away with using something as insidiously dangerous as the spike protein as the coding material for a nucleoside-modified RNA encapsulated LNP injection posing as a vaccine against SARS-2?

Just before I sign off, there are also signals that “they’re” going for another COVID-19 con in America. You can read about that here.

I had some words for Newsweek.

By the way, note how I ratio-ed the hell out of Newsweek and I only posted this a few hours ago. 1000/13,700*100 = 7.3% like ratio as opposed to their 838/348,300*100 = 0.2% like ratio.

THE PUBLIC SPEAKS LOUDLY.

Be aware. Be vigilant.

1. https://www.creative-biolabs.com/anti-glycan-antibodies/heparan-sulfate-heparin-structural-differences-biological-roles.htm

2. Clausen TM, Sandoval DR, Spliid CB, et al. SARS-CoV-2 infection depends on cellular heparan sulfate and ACE2. Cell. 2020;183(4):1043-1057.e15. doi:10.1016/j.cell.2020.09.033

3. Liu L, Chopra P, Li X, et al. Heparan sulfate proteoglycans as attachment factor for SARS-CoV-2. ACS Cent Sci. 2021;7(6):1009-1018. doi:10.1021/acscentsci.1c00010

4. Kalra RS, Kandimalla R. Engaging the spikes: heparan sulfate facilitates SARS-CoV-2 spike protein binding to ACE2 and potentiates viral infection. Signal Transduct Target Ther. 2021;6(1):39. doi:10.1038/s41392-021-00470-1

5. Kearns FL, Sandoval DR, Casalino L, et al. Spike-heparan sulfate interactions in SARS-CoV-2 infection. Curr Opin Struct Biol. 2022;76:102439. doi:10.1016/j.sbi.2022.10243

6. Yu J, Yuan X, Chen H, Chaturvedi S, Braunstein EM, Brodsky RA. Direct activation of the alternative complement pathway by SARS-CoV-2 spike proteins is blocked by factor D inhibition. Blood. 2020;136(18):2080-2089. doi:10.1182/blood.2020008248

7. Lo MW, Amarilla AA, Khromykh AA, et al. SARS-CoV-2 triggers complement activation through interactions with heparan sulfate. Clin Transl Immunology. 2022;11(8):e1413. doi:10.1002/cti2.1413

8. Kearns FL, Sandoval DR, Casalino L, et al. Spike-heparan sulfate interactions in SARS-CoV-2 infection. Curr Opin Struct Biol. 2022;76:102439. doi:10.1016/j.sbi.2022.102439

9. Yu J, Gerber GF, Chen H, et al. Complement dysregulation is associated with severe COVID-19 illness. Haematologica. 2022;107(5):1095-1105. doi:10.3324/haematol.2021.279155

10. Pires BG, et al. Hyper-inflammation and complement in COVID-19. Am J Hematol. 2023;98(Suppl 2):S27-S34

11. https://www.merriam-webster.com/medical/polyanion

12. Ferreira VP, Pangburn MK, Cortés C. Complement control protein factor H: the good, the bad, and the inadequate. Mol Immunol. 2010 Aug;47(13):2187-97. doi: 10.1016/j.molimm.2010.05.007. PMID: 20580090; PMCID: PMC2921957

13. Krauson AJ, Casimero FVC, Siddiquee Z, Stone JR. Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients. NPJ Vaccines. 2023 Sep 27;8(1):141. doi: 10.1038/s41541-023-00742-7. PMID: 37758751; PMCID: PMC10533894

14. Ota N, Itani M, Aoki T, et al. Expression of SARS-CoV-2 spike protein in cerebral arteries: Implications for hemorrhagic stroke post-mRNA vaccination. J Clin Neurosci. 2025;136:111223. doi:10.1016/j.jocn.2025.111223

15. search_terms <- c(“Endothelial dysfunction”,“Vascular disorder”,“Vasculitis”,“Vasculitis necrotising”,“Endarteritis”,“Arteritis”,“Thrombotic microangiopathy”,“Transplant associated thrombotic microangiopathy”,“Haemolytic uraemic syndrome”,“Atypical haemolytic uraemic syndrome”,“Thrombotic thrombocytopenic purpura”,“Microangiopathic haemolytic anaemia”,“Disseminated intravascular coagulation”,“Capillary leak syndrome”,“Systemic capillary leak syndrome”,“Renal vascular disorder”,“Glomerular vascular disorder”,“Hyaline occlusive glomerular microangiopathy”,“Pulmonary veno-occlusive disease”,“Pulmonary capillary haemangiomatosis”,“Endothelial cell injury”,“Vascular endothelial injury”)

16. https://en.wikipedia.org/wiki/Endothelium