Your nose bacteria are smarter than the entire vaccine industry

MenB vaccine risks, fear campaigns, and natural immunity for the win

Disclaimer:

I am a person who believes that every single person has inalienable rights and a duty to self-sovereignty. Therefore, I believe that anyone can choose to take whatever course of action they decide to take - including in the realm of vaccines - to assure their own well-being. But this choice has to be an informed one. I also firmly believe that no one has the right to tell another what to do as a course of action to assure their own well-being - especially in the realm of vaccines.

I also want to express how sad it makes me feel, after devoting my brain and my time and energy to the pursuit of knowledge in science for decades, that people appear to prefer profiteering to healing. From peer-review all the way to vaccine design and deployment. I must reiterate Mark Baum’s speech at the end of the movie in The Big Short with my own flair, because the words are simply too perfect not to use here to express how I feel. It’s more than a parallel.

Protection comes from a healthy, balanced microbiome and a well-tuned local immune response at the entry points, not mainly from systemic (blood-based) immunity or injected vaccines.

My thesis is pretty simple. Vaccinologists took a good idea, inoculation against pathogens to prevent severe disease in the context of dangerous pathogens, turned it into an atomic bomb of fraud and stupidity, that’s on its way to decimating world health. We live in an era of fraud; not just in vaccinology, but in banking, government, education, religion, food, even baseball. What bothers me isn’t that fraud is not nice or that fraud is mean, it’s that for 15,000 years, fraud and short-sighted thinking have never, ever worked. Eventually people get caught and things go south. When the hell did we forget this?

I thought we were better than this and the fact that we’re not doesn’t make me feel alright and superior. It makes me feel sad.

I want to elaborate and expand on an article I wrote yesterday called “Insane in the membrane - getting ahead of the meningitis fear curve - Don’t just get in line like you did last time, please”. It covered why and how the newer vaccines against meningococcal B strains consist of synthetic/recombinant versions of natural meningococcal lipoproteins (and how they may lead to Lyme disease-like symptomatology), are potentially dangerous and how in the past, meningitis vaccines actually led to meningitis.

In the previous article, I discussed the self-adjuvanting properties of bacterial triacyl lipoproteins (ie: Trumenba → lipidated Factor H-binding protein (FHbp)) and their ability to drive strong innate immune responses via TLR2. It is designed to be highly immunogenic. I argued that injecting bacterial triacyl lipoproteins into human bodies was a bad idea for very specific reasons, and urged caution against fear-driven uptake of [these] vaccines in favor of natural immunity and common sense.

In this article, I will focus on the recombinant protein antigens themselves - particularly FHbp - used in Bexsero (4CMenB; GSK) and Trumenba (MenB-FHbp; Pfizer) and how autoimmunity from the use of this protein should be expected, and not merely sloughed off as a mild and transient effect.

N.B. The article’s mechanistic details (FH as soluble plasma regulator, tick-over, C3b amplification, MAC pores, and how anti-FHbp antibodies “unhijack” the “shield”) apply to invasive disease in blood. However, they are not fully applicable to the mucosal compartment where initial bacterial colonization and control occur.

I will approach this from 3 points of view:

1. The mechanism of action of FHbp-based MenB vaccines and why they are potentially dangerous,

2. Why the recent meningococcal B “outbreak” was a part of the fear mongering playbook that we were all subjected to during the COVID con,

3. Why natural immunity is better in the context of Neisseria meningitidis with a focus on commensal vs. pathogenic Neisseria bacteria.

And awaaay we go!

1. The mechanism of action of FHbp-based MenB vaccines and why they are potentially dangerous

Bacteria are amazing organisms that have evolved clever strategies to hijack components of our immune systems in order to survive and colonize new “hosts”. (That would be us.) One of their most effective tactics is to borrow host molecules to protect themselves from immune destruction. And amazingly, these bacteria can share these survival mechanisms with other bacteria through horizontal gene transfer (organism to organism as opposed from mama to offspring).

A perfect example of this is when Neisseria meningitidis borrows human complement regulator, Factor H (FH) to avoid complement-mediated killing. The new meningococcal serogroup B vaccines, Bexsero and Trumenba, exploit this key FH-immune-evasion strategy of Neisseria meningitidis.

Figure 1: Scanning electron micrograph of a single N. meningitidis cell (colorized in blue) with its adhesive pili (colorized in yellow).. https://en.wikipedia.org/wiki/Neisseria_meningitidis

Fact 1: N. meningitidis uses its own surface protein FHbp (don’t forget this stands for Factor H-binding protein) to hijack the host’s own complement regulator, FH, thereby protecting itself from complement-mediated killing.

Fact 2: The vaccines contain recombinant FHbp and work by generating antibodies that bind to this bacterial protein, blocking its ability to recruit human FH and thereby restoring effective complement attack on the meningococcus.

Now I know that was a mouthful. Allow me elaborate.

First of all, what the hell if FH?

FH is a soluble glycoprotein and a member of the regulators of complement activation (RCA) family. It functions as a complement control protein and plays a critical role in regulating the complement system, particularly the alternative pathway.¹

Yes, it is important. To understand why, we first need to understand what the complement system is and why it plays such a critical role in our defense against pathogens via this system. Although the complement system is highly complex, grasping its fundamental functions is sufficient to appreciate how vital it is for protecting us from infection.

The complement system is a complex, tightly regulated cascade that forms a critical part of the innate immune system - our first line of defense against invading pathogens. Activation of the cascade ultimately leads to the formation of membrane attack complexes (MACs), which insert into the outer membrane of target pathogens (such as bacteria), creating pores that cause cell lysis. Complement activation also promotes phagocytosis by opsonizing pathogens and triggers localized inflammation to recruit immune cells.

The complement cascade can be initiated through three main pathways: the classical pathway, the lectin pathway, and the alternative pathway (as shown in Figure 2). For this article, the alternative pathway is the most relevant. Importantly, the alternative pathway is continuously activated at a low, spontaneous tick-over (low-level, spontaneous, continuous activation)² level, even in the absence of infection. It is akin to leaving your car idling while you buy your avocados.

Figure 2: Scheme of the complement system. https://en.wikipedia.org/wiki/Complement_system

One of the central players in the alternative complement pathway is C3b. As I discussed in a previous article, native C3 (the inactive precursor) is one of the most abundant complement proteins in human plasma, circulating at approximately 1.0–1.5 mg/mL (average ~1.2 mg/mL). In contrast, its activated form, C3b, is present only at very low levels under normal conditions. C3b is generated only when the complement cascade is triggered, and is rapidly inactivated if not stabilized on a surface.

So why is this relevant?

FH is the primary negative regulator of the alternative pathway of complement.³ It prevents uncontrolled complement activation and protects host cells from self-attack by the complement system. FH is also abundant in plasma, with normal concentrations typically ranging from 150 to 800 μg/mL (average ~200–500 μg/mL). It is mostly produced by hepatocytes in the liver, with additional local production by several other cell types, including endothelial cells, monocytes, fibroblasts, platelets, and retinal pigment epithelial cells. [2]⁴⁵ Because the alternative pathway undergoes continuous low-level tick-over activation, FH must be present throughout the body to distinguish self from non-self and to prevent complement-mediated damage to healthy host tissues.

Rehash: FH binds to C3b on host cell surfaces.⁶ FH indeed acts as a cofactor that recruits and enables a serine protease (FI) to cleave C3b into its inactive form. This mechanism prevents amplification of the alternative complement pathway on host cells and acts as the body’s endogenous native shield. Healthy human cells use FH, together with membrane-bound complement regulators, to distinguish self from non-self. By shutting down the alternative pathway amplification loop on their surface, they protect themselves from unwanted complement activation and self-attack. Figure 3 is a highly simplified visual of how our cells use this shield to prevent complement-mediated destruction (top left), how N. meningitidis hijacks this same system via FHbp (middle left), how the vaccine-generated antibodies against FHbp unhijack this complement protection strategy (bottom left) and how I believe this comes with problems leading to autoimmunity (right).

Figure 3: Representation of the inactivation of alternative pathway of complement in native setting, N. meningitidis setting and vaccine (Bexsero and Trumenba) setting (left panel). The schematic also shows the potential mechanism of action of auto-antibody generation to induce autoimmunity (right panel).

Rehash: The same elegant endogenous shield that protects our own cells from complement attack gets brilliantly hijacked by Neisseria meningitidis. The bacterium expresses the FHbp protein that binds human FH, coating itself with the host’s own regulator and thereby evading complement-mediated killing.

Let’s look more closely at the right panel in Figure 3. Imagine you inject a foreign bacterial protein, mutated or not. Your antigen-presenting cells pick it up, and the adaptive immune response kicks in, generating antigen-specific T and B cells. Those B cells eventually turn into plasma cells that pump out high-affinity antibodies against the FHbp antigen (in this case). At the same time, the complement system is quietly active in the background. Through tick-over, C3 spontaneously hydrolyzes at a low level, and any C3b that forms on surfaces is normally quickly inactivated. FH plays the starring role here: it binds to C3b and serves as a cofactor for FI, which cleaves C3b into its inactive form - namely iC3b - thereby shutting down the alternative pathway amplification loop on host surfaces.

The take-home message is this:

When you receive an FHbp-based meningococcal vaccine, two coordinated things occur. First, the immune system generates specific antibodies against FHbp. Second - and equally important - these antibodies activate the complement system (both classical and alternative pathways), which is the main mechanism that ultimately kills the bacteria.

What concerns me is the following:

Because FHbp is a protein that naturally binds human FH, the injected antigen can form FHbp–FH complexes in vivo. In addition to the intended anti-FHbp antibodies, a small proportion of the antibody response may be directed against epitopes of the FHbp–FH complex. This might lead to the generation of low-level antibodies that cross-react with human FH (anti-FH antibodies). Since FH is an endogenous human protein, the risk is that such autoantibodies could interfere with its normal regulatory function and potentially disrupt complement control on host cells.

See the problem?

If these autoantibodies bind to FH - whether in its soluble form in plasma, or when bound to host cell surfaces - they could locally disrupt the regulatory function of FH, thereby impairing its ability to control the alternative complement pathway and potentially leading to uncontrolled complement activation.

This is not simply what could happen. It has been demonstrated to happen in the literature in both animal models and humans. By Sharkey, in the case of the latter. I love that surname.⁷⁸⁹ I whole-heartedly believe this requires further study, and indeed, long-term studies.

The typical response to this particular anticipated problem from legacy dudes (big pharma) is that it’s “no problem” because the generation of the anti-FH antibodies is described as small and transient - aka: “mild and transient”. Now perhaps this is true and there’s nothing to worry about, but I am skeptical because I have heard and seen these words “mild and transient” used before.

2. Why the recent meningococcal B “outbreak” was a part of the fear mongering playbook that we were all subjected to during the COVID con

Everybody who hasn’t had their head in the sand has heard the phrase “mild and transient”. It was (and still is) used to describe myocarditis reported in temporal proximity to injection with the COVID-19 injectable products. But let’s be clear: those two words are deeply misleading when applied to inflammation of the myocardium, in general. When heart muscle cells (myocytes) are damaged, they are replaced by non-contractile scar tissue. The myocardium is meant to be flexible and electrically conductive so the heart can pump efficiently. Once that living, flexible tissue is replaced by stiff, non-conductive scar, the heart cannot function as it was designed to. Period. In children and young adults - the groups most commonly affected - this means potentially lifelong, irreparable damage. That is neither mild nor transient, especially if spike protein production persists.

I simply don’t trust the vaccine industry anymore. The brilliant scientists working at the bench are too far removed from the real-world consequences of their work once it becomes a final product - especially in the context of vaccines. There’s too much financial investment, too much focus on stock prices and profits, and far too little concern about whether the product actually works without causing harm. That’s just the truth, and it’s gross.

So when I see the words “mild and transient” attached to the idea of autoimmunity following vaccination - particularly with newly emerging vaccines - I shudder. These products should undergo many generations of rigorous testing before they ever go near a human being. Or even an animal, for that matter. Think self-amplifying RNA-LNP injections.

The impetus for my first article on the meningitis vaccine was the so-called Kent “outbreak”, which I believe was never a genuine outbreak at all, but rather theatre following the same familiar script we saw throughout the COVID-19 pandemic. Yesterday, Joel Smalley published a brilliant article in which he made one of the most powerful points I’ve heard about science - including vaccine science. He highlighted that Martin Neil (a fellow scientist →Bayesian analyst) and I had independently reached exactly the same conclusions about these particular vaccines (and the theatre), despite using entirely different methods, being from completely different fields, and without any communication. We hadn’t spoken (me and Neil, nor me and Joel) for years, and had no idea the other was even working on the same question, yet we arrived at precisely the same conclusion.

The Kent Meningitis Scare

Convergence is even more powerful than reproducibility, in my opinion.

I immediately saw this “Kent event” as a replay of the COVID-19 playbook - a fear-mongering campaign designed to drive as many young people as possible to get vaccinated with a product that could end up doing more harm than good. While many did line up for the vaccine, a significant number pushed back, and I believe this resistance ultimately contributed to the reversal of the playbook narrative. You can read more about that here and here.

“The lack of new cases is a good sign and may signal that the Kent outbreak has been contained,” said Simon Williams, a public health expert at Swansea University.¹⁰

Meanwhile, health officials in Kent said that the peak of the outbreak may have passed, with no new meningitis cases reported over the weekend.¹¹

Yeah. Sure. It wasn’t an outbreak. It was a few cases, and even if there was an emergent subtype, if you read Joel’s article, you’ll see that the playbook writes itself in that:

The early inflated case counts, [Neil] argues, are not a failure of execution but a predictable consequence of the surveillance design itself. The later “downgrading” of cases is not reassuring correction - it is the system catching up with its own false-positive rate.

Yup. Even the European Centre for Disease Prevention and Control aren’t concerned. I am not trying to imply that meningitis isn’t worrisome in general - it is. Neisseria meningitidis is a pathogenic strain of Neisseria and can mess you up. But don’t worry! Nature has already sussed this problem out and has an elegant solution.

And this provides the perfect segue to the last section of this article.

3. Why natural immunity is better in the context of Neisseria meningitidis with a focus on commensal vs. pathogenic Neisseria bacteria.

We are chock full of all sorts of things like bacteria, viruses, fungi and more! In fact, microbial cells make up a significant portion of what lives on and inside us, yet we remain fit as fiddles. This is because of many a reason, but in the context of bacteria, it is because many are commensal by nature. This means that we live with them and they don’t bother us and we don’t bother them. Happy balance.

Commensal bacteria colonize our bodies (including the nasopharynx) without causing harm, and in turn, we provide them with a comfortable environment. In fact, Neisseria meningitidis lives harmlessly in the nasopharynx of up to 40% of healthy people as a commensal! Another beautiful example of balance at play in this mucosal compartment is Neisseria lactamica, a harmless relative of Neisseria meningitidis that also commonly colonizes the human nasopharynx, especially in children and adolescents. When it colonizes the nasopharynx, it can stimulate cross-reactive antibodies that offer some degree of protection against its more dangerous cousin, Neisseria meningitidis.

Nature’s quiet trade-off.

Once again, this is not only my idea; this is published.¹²¹³¹⁴¹⁵¹⁶ Immunity to the harmless commensal Neisseria lactamica confers cross-protection against the pathogenic Neisseria meningitidis because the two species share many highly conserved surface antigens (including outer membrane proteins, lipooligosaccharide structures, and other epitopes), so antibodies generated against N. lactamica during asymptomatic nasopharyngeal colonization cross-react with N. meningitidis, enabling complement-mediated killing and preventing colonization or invasive disease by the meningococcus.

The bottom line is that supporting a healthy commensal microbiome can help maintain balance and, in certain cases, contribute to protective immunity.

Update: Neisseria meningitidis only rarely escapes to cause catastrophic invasive disease (sepsis or meningitis). This escape is uncommon - roughly 1 in 25,000 carriers develop disease in endemic periods - and usually requires a combination of bacterial, host, and environmental factors that disrupt the normal balance at the mucosal surface. When escape happens, the bacteria can enter the blood and big problems can ensue including sepsis.

So, in a healthy and balanced setting, N. meningitidis is simply kept in check. Catastrophic illness happens when this balance is compromised and/or a sufficiently fit bacterial variant (or subtype) exploits the opening to cross into the blood, where it can multiply rapidly if complement/antibody defenses are not ready. This is the reason why most carriers stay healthy, why disease is sporadic and unpredictable, and why supporting overall mucosal and microbiome health is emphasized over relying solely on systemic (injected) immunity.

I would be remiss if I didn’t also mention the gut microbiome players (including species such as Bifidobacterium - shout-out to Sabine Hazan!) that play important roles in overall health. It may also have a direct influence on nasopharyngeal colonization and/or meningococcal immunity (I’ve heard weirder ideas), but this remains an area of active research rather than established fact.

So did I punch three holes in the fabric vaccinology?

I think I did.

Update - March 25, 2026

Reply from the great Robert Clancy - the Godfather of mucosal immunity

I got an email from the amazing Dr. Robert Clancy where he delightfully contributes to my own bird’s eye view of the biology of colonizing bacteria, and indeed the biology of compartments and the interaction between them. Indeed my goal was to shit on the MenB vaccine as in IV “solution” to a mucosal “problem”, but there are a couple clarifications I would like to stress here that I don’t think I adequately addressed in the original draft of my article. This is why I love Substack!

In direct response to his excellent points, an addendum, if you please.

1. Complement is relevant but secondary at mucosa. Local complement (produced by epithelial cells) aids opsonization/inflammation in secretions, yet mucosal protection against carriage often proceeds without it (as shown in animal models where complement depletion does not increase colonization).

2. Vaccines like Bexsero/Trumenba primarily induce systemic serum bactericidal activity for invasive disease prevention; they are weaker at inducing strong mucosal immunity (ie: secretory IgA or Th17 cells) that limits initial colonization. This is why using IV vaccines against things involving the nasal mucosa is a stupid idea: they, at best, target only ‘escaped’ bacteria, as Dr. Clancy so beautifully described.

   1. Mucosal surfaces (nose/throat) are defended by a compartmentalized immune system favoring local IgA, tissue-resident memory cells, and microbiome interactions. Systemic vaccines are aimed at blood/tissue protection (preventing invasive disease), but fail to block initial colonization/transmission at the entry site. This is a known limitation for many respiratory/mucosal pathogens (ie: similar patterns seen with some flu and COVID-19 shots).

   2. Natural carriage (especially with commensal Neisseria lactamica) induces cross-protective responses at the mucosa via shared antigens, often independent of strong complement reliance - supporting microbiome + local cellular immunity as key for resilience.

3. Dr. Clancy also noted his interest in the emergent subtype that I breezed over in the original draft. This subtype has been circulating in England since around 2020. It was described as having a “clearly distinct genome” with “potentially significant genetic differences” that could influence how infectious or virulent the strain behaves. UKHSA noted it is a “realistic possibility” that these changes helped drive the unusually rapid and large cluster. I decided to add this as point 3 to the addendum because I am suspicious about where this subtype came from (or who made it). Sorry, but I am.

By the way, as noted by The Cat in the Hat on X, right in the middle of the Kent “outbreak”, the WHO took their meningococcal meningitis page offline for 4 days. When it reappeared, the word “aerosol” had magically vanished. No why would they have done that?

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3. Moore SR, Menon SS, Cortes C and Ferreira VP (2021) Hijacking Factor H for Complement Immune Evasion. Front. Immunol. 12:602277. doi: 10.3389/fimmu.2021.602277

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8. Giuntini S, Beernink PT, Granoff DM. Effect of complement Factor H on anti-FHbp serum bactericidal antibody responses of infant rhesus macaques boosted with a licensed meningococcal serogroup B vaccine. Vaccine. 2015;33(48):6629-6635. doi:10.1016/j.vaccine.2015.10.036

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10. https://www.theguardian.com/society/2026/mar/23/meningitis-no-new-cases-linked-fatal-kent-outbreak-ukhsa

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