Are the mRNA vaccines weakening children's immune systems?

It seems the immune system is a lot more complex than we make it out to be.

As the war over the COVID vaccines rage on, and as fear over rising COVID cases make their way into the media, a push for further COVID vaccination looms with even possible vaccine mandates making a return.

As I stated previously, at this point it’s not so much that people may dive right into getting more boosters, but rather at this point most people may just be done with the whole performative charade overall and would rather just move on with life.

Nonetheless, there is still a lot left to be elucidated when it comes to these vaccines, including the extent of their possible harmfulness.

Over the past week several people have covered a recent study¹ which seems to highlight a possible concern with these mRNA vaccines, in that they may possibly weaken the immune system of vaccinees.

This comes after a preprint was published in March 2023² which seems to parallel the results seen in this recent study.

In short, there’s a growing body of work that suggests that vaccines and infections can influence how we respond to future infections. Although it’s been previously thought that the innate immune system is static (i.e. it cannot be modified), the literature does seem to suggest that the innate immune system itself can be altered by way of various pathogens.

Some of this may be direct depletion of immune cells, such as what appears to be the case in measles where immune depletion is seen months to days after an infection and may contribute to non-measles related mortalities.³

And indeed, lymphocytopenia from SARS-COV2 infection also suggests a possible way in which secondary infections may contribute to mortality. A recent study published in Cell⁴ also notes the possibility of epigenetic changes to innate immunity after severe COVID infections, which may be related to Long COVID. However, note that in this study this correlation seems to be related to persistent cytokine production in acute COVID infection and possible alterations in immune responses due to these cytokines.

I haven’t read this study yet so take these assertions with a good deal of skepticism. Nonetheless, what this tells us is that the immune system seems to be in a constant state of ebb and flow, being influenced by the insults we throw at it. It’s a lot more complex than expecting an all-around robust immune response to any pathogen, and instead infers that the immune system may direct, or possibly pick-and-choose how to go about dealing with these foreign substances.

Consider that, in contrast to these mRNA findings, studies seem to suggest that the adenoviral vector vaccines seem to enhance cytokine responses, suggesting a possible secondary immunity boost in these vaccines.⁵,⁶ There also seemed to be some remarks suggesting a reduction in all-cause mortality in those who were given the adenoviral vector vaccines, although I haven’t looked into these assertions.

These effects are referred to as “non-specific” effects, as they aren’t effects directly tied to the pathogen in question (SARS-COV2), but are nonetheless influenced by vaccination against said pathogen.

So this raises a question of why this discrepancy is occurring. On the surface, it could be related to demographic differences (the current study occurred in children in contrast to the adults in the mRNA preprint and adenoviral study).

The LNPs and pseudouridine nature of the mRNA vaccines may circumvent immune responses, and therefore lead to a reduced inflammatory response relative to an infection, although the adjuvant-nature of the LNPs seem to also be highly inflammatory, making the scenario more complex and requiring contextualization to determine which inflammatory biomarkers may be up or downregulated after vaccination relative to infection.

However, there’s a large possibility that this difference in immune responses is also due to the nature of the adenoviral vector vaccines, which inherently utilizes a different virus and requires transcription and translation in host cells. This is a more complex process that may mimic an active viral infection, which could induce a more robust inflammatory response as the other genes within the adenoviral vaccines, as well as the viral vector itself, are likely to both be immunogenic.⁷

So there’s a possibility that either the mRNA vaccines are immune weakening, or it’s quite possible that they are immune “lazying”, such that their spike presentation doesn’t serve as a similar parallel to an infection, and therefore the immune system doesn’t need to work as much.

This was remarked on in Dr. Maryanne Demasi’s Substack where she provides quotes from epidemiologist/professor Dr. Christine Stabell Benn, suggesting that inactivated virus-based vaccines may show greater all-cause mortality relative to live, attenuated vaccines, again likely emphasizing the point that the immune system likely has to work in order to stay strong.

New research shows mRNA jabs could weaken immune responses

“We found in our work that three months after subjects received the DTP vaccine, they showed lower immune responses in vitro to other infectious stimuli,” said Stabell Benn.

“Essentially, the immune cells become lazy, and they simply don't respond as vigorously when they are challenged with an infectious agent,” she added.

The opposite was true when “live” vaccines were administered to people, such as the BCG (tuberculosis) vaccine.

“After BCG vaccination, immune cells would react more actively in response to other bacterial stimuli by reprogramming cells in the bone marrow to spit out more active innate immune cells,” said Stabell Benn.

DTP is a combination vaccine which targets diphtheria, tetanus, and pertussis, and generally includes the toxoids (toxic agents) of diphtheria and tetanus while using either a killed bacterial or the antigens from the bacteria that causes pertussis.

In contrast, BCG is a live, attenuated vaccine of Mycobacterium bovis, the bacterial agent in tuberculosis.

Because this vaccine has an active, albeit weakened, strain of the bacteria it seems to produce a broader immune response relative to pure antigen presentation given its ability to still be infectious. Several bits of literature have come out suggesting possible heterologous effects of BCG vaccination in immunity.⁸

Interestingly, a study from 2021⁹ published in Nature looked at immune profiles in those given the inactivated SARS-COV2 vaccine Vero Cell. I haven’t looked at the study in detail, but cursory examinations seem to suggest that the inactivated viral vaccine led to a response “similar to an infection”, which appeared to include signs of immune deficiency:

Moreover, the gene set positively contributing to MVS scores, also known to be associated with severe symptom development, was highly expressed in monocytes. Type I interferon (IFN-α/β) responses, supposedly beneficial against COVID-19, were downregulated after vaccination. In addition, the negative MVS genes were highly expressed in lymphocytes (T, B, and NK cells), yet showed reduced expression after vaccination. Together, these data suggested that after vaccination, at least by day 28, other than generation of neutralizing antibodies, people’s immune systems, including those of lymphocytes and monocytes, were perhaps in a more vulnerable state.

So again, there’s a curious question of whether the mRNA platform itself carries a risk of immune deficiency, or if the immune system isn’t made to respond to simulacrums, and instead operates better when challenged.

In the case of the COVID vaccines there doesn’t appear to be any attenuated viruses in use, although the Novavax platform may provide some insights into these immune responses. That is, if Novavax appears to show an immunological response similar to the mRNA and inactivated viruses then it may suggest that some form of an active infection may be needed to induce broader immune responses.

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Thinking in context

I will save the assessment for the Noé, et al. study for another time. In the meantime, note that, Aside from a small sample size, the study utilized children that were enrolled into a BCG vaccine trial in which non-specific effects of infant BCG vaccination was measured. It appears that many of the children enrolled into the Noé, et al. were children who were not given a BCG vaccination in the BCG study:

Of the 47 children who provided a blood sample at V1, 21 were female and 32 did not receive BCG in the MIS BAIR trial.

I’m not sure to what degree this point is relevant when it comes to the Noé, et al. study, but given that the entire point of this article is to emphasize that prior vaccinations and infections may mold our future immune responses, then it may be worth considering whether BCG vaccination may have had any effect on the results of this trial. Keep in mind that lack of vaccination in the MIS BAIR trial does not mean these children never received BCG at some future point in time.

Note that this trial itself also doesn’t provide an accurate measure of future infections. That is, it utilized isolated cells and determined their response to antigens or heat-killed bacteria, and so the study itself doesn’t mimic a proper infection. It’s also worth considering, given the naïve history of these children’s immune profiles, if the responses in these studies are due to lack of prior exposure to these pathogens given that the study would inherently show a bias towards SARS-COV2 responses if exposed to SARS-COV2 antigens.

It’s always important to assess information from the perspective of figuring out what exactly the study would mean in a general sense. Consider what information you would need to draw conclusions of whether the mRNA vaccines are causing immune deficiencies, or what evidence would refute this argument.

A good example would be to compare infection rates in this vaccine group relative to a non-vaccinated group and measure immune profiles post-secondary infections. Unfortunately, since this study was conducted in Australia there was no viable control group since it was considered “unethical” to not vaccinate any children:

Limitations include the inability to include an unvaccinated control group due to the ATAGI recommendation for all children aged 5 to 11 years to receive the BNT162b2 vaccine. It was unethical to randomise children into an unvaccinated, placebo or delayed vaccination group, given that ATAGI recommended the BNT162b2 vaccine for the age group of interest and that Melbourne was experiencing a surge in COVID-19 cases in the community during the study period.

It would be critical information to figure out whether children experience increased rates of infection, or if the immune system is more malleable and not “fixed” after COVID vaccination.

Put another way, are children vulnerable to more infections after vaccination, but then “recover” their immunity afterwards? Again, this is something that would need to be studied.

All of this does, however, raise a question of whether the increase in childhood infections are due to the immune deficiency from the vaccines, due to immunity debt, or due to other circumstances. In general, it seems that the body needs to be challenged in order to become more resilient, and it’s apparent that everything that has gone on the past few years have worked against strengthening our immune systems.

Our immune system is a lot more complex than we make it out to be, and even now more information comes to light about facets that we did not know about, which is again why more research and better studies are always needed in order to gain better context.

Note: It is, however, interesting to think about these immune deficiencies within the context of HHV reactivation, which I have covered previously. It’d be interesting to consider the course of HHV reactivation and attenuation within the context of these possible immune deficiencies:

The role of HHV reactivation in everything going on...

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1. Noé A, Dang TD, Axelrad C, Burrell E, Germano S, Elia S, Burgner D, Perrett KP, Curtis N and Messina NL (2023) BNT162b2 COVID-19 vaccination in children alters cytokine responses to heterologous pathogens and Toll-like receptor agonists. Front. Immunol. 14:1242380. doi: 10.3389/fimmu.2023.1242380

2. The impact of BNT162b2 mRNA vaccine on adaptive and innate immune responses

Konstantin Föhse, Büsra Geckin, Martijn Zoodsma, Gizem Kilic, Zhaoli Liu, Rutger J. Röring, Gijs J. Overheul, Josephine S. van de Maat, Ozlem Bulut, Jacobien J. Hoogerwerf, Jaap ten Oever, Elles Simonetti, Heiner Schaal, Ortwin Adams, Lisa Müller, Philipp Niklas Ostermann, Frank L. van de Veerdonk, Leo A.B. Joosten, Bart L. Haagmans, Reinout van Crevel, Ronald P. van Rij, Corine GeurtsvanKessel, Marien I. de Jonge, Yang Li, Jorge Domínguez-Andrés, Mihai G. Netea

medRxiv 2021.05.03.21256520; doi: https://doi.org/10.1101/2021.05.03.21256520

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7. Remember that the viral vector used had to be one that does not widely circulate among humans. Hence, why a chimp adenovirus was used by Oxford/AstraZeneca (giving it the name ChAdOx1) while J&J used Ad.26 which is rather rare strain in humans.

8. Butkeviciute, E., Jones, C. E., & Smith, S. G. (2018). Heterologous effects of infant BCG vaccination: potential mechanisms of immunity. Future microbiology, 13(10), 1193–1208. https://doi.org/10.2217/fmb-2018-0026

9. Liu, J., Wang, J., Xu, J. et al. Comprehensive investigations revealed consistent pathophysiological alterations after vaccination with COVID-19 vaccines. Cell Discov 7, 99 (2021). https://doi.org/10.1038/s41421-021-00329-3