Sometimes a paper on a new method delivers a side punch to current understanding. Nothing in the title hints at this, and the authors deliver the critical blow en passant.
Over a 40-year career in microbiology I’ve met several cases. For example, the scientist who found a problematic type of antibiotic resistance to be extremely prevalent in Pakistan. This exercised him not one jot, despite obvious implications for treatment and for import into the U.K. What motivated Joe, whose name I’ve changed, was perfecting a test to detect bacteria with this resistance. One of his collaborators (a former colleague, I think) just happened to be in Pakistan, which proved – owing to the high prevalence of the resistance – to be the ideal testing ground.
Some scientists don’t want the trouble that comes from a disturbing result, especially when they have a new method to publicise. They fear the opprobrium reserved for heretics and disruptors. At best, controversial observations delay your paper’s publication. At worst, they lead to it being rejected. Why court trouble, especially if you have patents or intellectual property claims? More simply, some, like Joe, just have a ‘techno’ mindset. If they discovered a Roman mosaic whilst digging the garden they’d fixate on how it’d affect the roses.
Now, consider this paper, published a few days ago: ‘Nanocarrier imaging at single-cell resolution across entire mouse bodies with deep learning’ by Luo, J., Molbay, M., Chen, Y. et al in Biotechnol (2025).
The title suggests that it’s a paper for imagers and radiographers. The abstract – where you summarise the main points – outlines how ‘Single Cell Precision Nanocarrier Identification’ visualises the tissue distribution of encapsulated drug formulations, notably including those using lipid nanoparticles (LNPs). Even when dosages are tiny the method can reveal individual cells that the particles reached. The LNPs’ distribution is very wide, and the resolution very impressive. The end of the Discussion – where you reiterate key discoveries – stresses how the method may help pharmaceutical developers identify carriers that distribute only to the desired tissues. Examples are presented.
This is high-quality work, nicely described. Nothing I write here should be construed as a criticism. But, mid-Abstract, there’s the by-the-bye killer punch, describing a step used to validate the method. With my additions in brackets, it reads:
We demonstrate that intramuscularly-injected LNPs (lipid nanoparticles) carrying SARS-CoV-2 spike mRNA reach heart tissue, leading to proteome (i.e., protein expression) changes, suggesting immune activation and blood vessel damage.
The Results tell the detail. Luo et al confirm the wide tissue distribution of LNPs following intramuscular injection of mice. On the positive side, they concentrate in lymph nodes, which should promote an immune response. More concerningly, they also reach the heart. And, once the LNPs were loaded with the relevant mRNA, this prompted production of the SARS-CoV-2 spike protein, principally by the endothelial cells of the heart capillaries.
When mice were given intramuscular LNPs with no mRNA, 240 capillary endothelial cell proteins were up-regulated and 135 down-regulated. These numbers swelled to 578 and 201, respectively, once the LNPs were loaded with mRNA for SARS-CoV-2 spike protein.
Proteins that were up-regulated or down-regulated only with the spike mRNA present included those involved with protein and RNA metabolism and the immune response. And – more concerningly – those involved in the formation and maintenance of the blood vessels. Some correspond to those which, in humans, are associated with the Vascular Function Score, a predictor of stroke and heart attack risk. More generally, dysfunction of capillary endothelial cells is a marker for cardiac disease and a European Society of Cardiology Working Group describes them as “Sentinels of cardiac health”.
As the present authors put it: “The observed LNP accumulation and proteome changes in heart tissue suggest a potential mechanism by which LNP-based mRNA vaccines could contribute to the reported cardiac complications.”
Quite.
There are caveats. As the authors acknowledge, their LNPs may differ from commercial vaccines, maybe affecting behaviour. Nonetheless, they specifically show that LNPs formed with the ionizable lipid SM-102, as in Moderna’s vaccine, reach the heart as do more standard LNPs, resembling those used by BioNTech.
What the authors omit to explore, but which I will add for them, follows from the fact that they administered a single shot of LNPs containing native mRNA. After six hours or three days they then killed the mice and examined LNP distribution and protein expression, respectively.
Native RNA is readily degraded. It gives a burst of protein synthesis, then is digested and lost. By contrast, human Covid mRNA vaccines use RNA with one of its four component bases, uridine, replaced by methyl-pseudouridine. This increases stability and tolerability. Unlike native mRNA, methyl-pseudouridine-mRNA can persist in tissues for 30 days or longer. And, unlike Dr Luo’s mice, many humans have accepted multiple mRNA boosters, repeating this exposure.
If the damage to capillary endothelial cells reflected direct toxicity from the LNPs’ mRNA, then human vaccines, with modified mRNA, might evade the problem. If, on the other hand, damage is due to the spike protein, translated from the mRNA, then human vaccines are likely to be more harmful, owing to longer and repeated exposure. The latter scenario seems the more likely. When Luo’s LNPs were instead loaded with mRNA encoding EGFP – a useful-for-imaging fluorescent protein from jellyfish – many metabolic proteins again were up- and down-regulated. But, unlike with the spike mRNA, there is no intimation that these included any associated with vascular damage. Moreover, many studies point to the spike protein’s inherent toxicity.
In short, besides developing an elegant method – the focus of their paper – Luo et al show that LNP-encapsulated mRNA reaches the heart. Once there, it causes local production of spike protein. Cardiac endothelial cell damage ensues, most likely owing to the toxicity of the spike protein itself. This tallies with cardiac harm in a proportion of human vaccinees. Human exposure to spike protein is longer than in Luo’s mice and repeated, owing to the use of modified mRNA and to boosting. It is reasonable to fear that this multiplies the risk of cardiac damage.
Many of the vaccine-injured were vaccinated needlessly. They were too young to be at risk from Covid. And since the vaccine didn’t stop them catching Coid, altruistic vaccination by the young did nothing to protect their elderly contacts. The failure to stop transmission was evident by summer 2021, by which time there also were many reports of cardiac harm. Yet the push for universal vaccination, including of children, continued though the autumn and winter, with increasing coercion. The recklessness of these policies is now laid bare, down to the individual cell.
Fortuitously, Lady Hallett’s Covid Inquiry is discussing vaccine harms this very week. Can she, for once, move at the ‘Speed of Science’ and add Luo’s crucial observations to the agenda as an emergency item?
David Livermore was a professor of medical microbiology at the University of East Anglia.
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