A Curious Matter of Timing: How Annual COVID mRNA May Enable Constant Endothelial Inflammation/Microclotting (SPED)

As soon as the Spike Protein factories that mRNA induces begin to shut down, they are given a “booster” to keep production going.

Representative confocal microscopy images for qualitative analysis of co-localization of fluorescein labeled fibrin(ogen) and Cy5 labeled Spike amyloid. Top panels illustrate samples where fibrinogen has been co-incubated with Spike amyloid prior to plasmin degradation. Lower panel illustrate the degree of co-localization between Spike amyloid fibrils and thrombin induced fibrin.

It has been almost five years since I predicted that the Spike Protein of SARS-CoV-2 would induce what I eventually called SPED (Spike Protein Endothelial Disease). In December of last year, this was described almost precisely as I envisioned in a research article.

In this study, we investigated the scope of the vascular inflammatory effect of SARS-CoV-2 spike protein on phenotypic, functional, and transcriptional levels in both lung microvascular and aortic ECs. To provide a more comprehensive insight into the profile of vascular inflammation, we included a comparison with the inflammatory cytokine TNF-α, which is known to induce prolonged activation of ECs [47, 48]. Consistent with previous findings, our study revealed that SARS-CoV-2 spike protein triggered prolonged cell adhesion marker expression and cytokine/chemokine releases, along with increased immune cell binding and formation of a procoagulant state of the ECs [20, 22, 46, 49,50,51]. We observed a similar degree of vascular inflammation by SARS-CoV-2 spike protein to that with TNF-α. However, distinct gene activation profiles were found for the viral spike protein. We also showed that on the transcriptome level, SARS-CoV-2 spike resulted in sustained inflammation, changes in antigen presentation, and coagulation state of the endothelium. The observed prolonged effects beyond the presence of the spike protein suggests possible long-term consequences of SARS-CoV-2 on the endothelium.

Sustained Vascular Inflammatory Effects of SARS-CoV-2 Spike Protein on Human Endothelial Cells
https://link.springer.com/article/10.1007/s10753-024-02208-x#Sec20

I also predicted that this would result in damage to the microvasculature via microclotting, which would in turn damage organs and tissues. This was shown to be the case in a paper published July 1^st.

An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis has previously been made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein displayed a resistance to plasmin-mediated lysis. Here we investigated the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five out of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen-fibrin-fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601-620) impaired thrombin mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On contrary fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685-701) exhibited a marked resistance to plasmin mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks, as well as incorporate fibrin into aggregated structures that resist fibrinolysis. These results demonstrate how the Spike protein of SARS-CoV-2 could contribute to the formation fibrinolysis-resistant microclots observed in long COVID.

SARS-CoV-2 spike protein amyloid fibrils impair fibrin formation and fibrinolysis
https://www.biorxiv.org/content/10.1101/2025.06.30.661938v1.full

So, we know for certain now that the Spike Protein damages the endothelium and then that damage denies oxygen and nutrients to organs and tissues which, in turn, damages them. Clearly, the presence of the Spike Protein in the body is something which should be avoided.

We were told that the COVID vaccine mRNA, which produces the Spike Protein, was only localized and would not spread beyond the site of injection. I knew – and I am certain you did, too – that this was pure and absolute hogwash. Indeed, within a few years researchers began discovering that the mRNA was everywhere – and doing immense damage, even lethal damage.

The distribution and duration of SARS-CoV-2 mRNA vaccine persistence in human tissues is unclear. Here, we developed specific RT-qPCR-based assays to detect each mRNA vaccine and screened lymph nodes, liver, spleen, and myocardium from recently vaccinated deceased patients. Vaccine was detected in the axillary lymph nodes in the majority of patients dying within 30 days of vaccination, but not in patients dying more than 30 days from vaccination. Vaccine was not detected in the mediastinal lymph nodes, spleen, or liver. Vaccine was detected in the myocardium in a subset of patients vaccinated within 30 days of death. Cardiac ventricles in which vaccine was detected had healing myocardial injury at the time of vaccination and had more myocardial macrophages than the cardiac ventricles in which vaccine was not detected. These results suggest that SARS-CoV-2 mRNA vaccines routinely persist up to 30 days from vaccination and can be detected in the heart.

Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients
https://pubmed.ncbi.nlm.nih.gov/37758751/

So, we then knew the mRNA could persist for up to 30 days. But was this the limit? We were told it would be disintegrated by the body within days, but thirty? Turns out, it can go on for longer. Far, far longer. On April 3^rd of this year, we learned it can persist for as long as 17 MONTHS.

Spike protein expression was detected in 43.8 % of vaccinated patients, predominantly localized to the intima of cerebral arteries, even up to 17 months post-vaccination. While no active inflammatory changes were identified, infiltration of CD4-, CD8- and CD68- positive cells was observed in the spike protein positive vessels. In situ hybridization confirmed the presence of both vaccine-derived mRNA and SARS-CoV-2 virus-derived mRNA, which encode the spike protein, in select cases. Notably, spike protein positivity was observed exclusively in female patients (P = 0.015). None of the cases showed nucleocapsid protein positivity, supporting the absence of active viral infection.

Expression of SARS-CoV-2 spike protein in cerebral Arteries: Implications for hemorrhagic stroke Post-mRNA vaccination
https://pubmed.ncbi.nlm.nih.gov/40184822/

Why is this important? Because both vaccine-derived mRNA and virus-derived mRNA were found in the cerebral arteries. If the mRNA is persisting for up to 17 months, then there is the potential for endothelial damage and inflammation to continue and never cease. How? Recurring infections and – boosters. It would seem to be madness to keep reintroducing a protein into the body which causes such widespread damage and inflammation on a yearly basis. Espceially when it can persist for almost a year and a half. I don’t wish to cast aspersions, but, if you wanted to push the elderly (or any of us) towards a quicker end, recommending hyperaccelerated inflammaging and vascular damage every year would certainly do the trick.

The insanity must end.

I will continue to work towards understanding and healing. Thank you, as always, for your continued support, dialogue and readership. Please have a blessed week and be hopeful.