Why may an increased exposure to SARS-CoV-2 improve immunity?

In July of 2021, I published a blog on my website titled, ‘The vaccinated getting infected marks the end of the pandemic’. In it, I wrote that we were seeing a rise in COVID-19 cases, particularly amongst those who have been double jabbed because those who have been vaccinated have antibodies only to the vaccine-coded-spike proteins. Something we have discussed earlier in this book. 

“Viruses have a tendency to mutate and preferentially at the spike though, rendering vaccines somewhat useless against newer more mutated forms of the virus, e.g. delta.”, I wrote. 

And continued with, “If natural immunity is far superior at reducing re-infection and if circulating strains of the virus are less harmful than before, then it would make the most sense now to allow everyone to restart life back as usual. Everyone should be exposed to the virus naturally so we can all build long-lasting robust immunity to it. We must aim to naturally improve people’s immune systems through diet and lifestyle (something we should have been doing for the last two years). No need for boosters, no need for lockdowns, no need for masks, for which the evidence for effectiveness is poor anyway.”. 

Nothing changed after writing that. People queued up for their boosters. I wasn’t surprised. 

A year later, my sentiment still stands, and the evidence that these vaccines are more useless than natural infection against newer strains holds up to scientific scrutiny too. Here, one paper notes

“Together, our results indicate that Omicron can evolve mutations to specifically evade humoral immunity elicited by BA.1 infection. The continuous evolution of Omicron poses great challenges to SARS-CoV-2 herd immunity and suggests that BA.1-derived vaccine boosters may not be ideal for achieving broad-spectrum protection.”

It seems like the best approach to protect yourself against rapidly mutating respiratory viruses is repeated mucosal exposure in one’s respiratory tract. 

The mucosa, also known as the mucous membrane, is the membrane that lines various cavities in the body and covers the surface of internal organs. It is made up of epithelial cells and the substances they secrete. Basically, it’s the surface layer that covers our eyes, mouth, throat, tongue and the rest of our insides, that separates us from the outside world. 

Those surfaces are our main sites of infectious threat since various microorganisms and allergens in our environment invade through the nose, mouth, eyes and gut all the time. To keep these dangerous buggers out, we have evolved the mucosal immune system,  the largest component of the entire immune system. 

The mucosal immune system consists of innate and adaptive immunity components that are found in circulating blood, but what (amongst other things) makes the mucosal immune system unique are secretory IgA (SIgA) antibodies and a special set of T cells called resident memory T (TRM) cells. 

SIgA is the major antibody in mucosal secretions.  SIgA in the mucosa cannot kill pathogens nor activate the complement system. It works by attaching to the microorganism and then eliminating them from the upper respiratory tract through coughing up phlegm (mucociliary transport). And though an antibody, SIgA is considered a component of the innate immune system. An important fact to note also is that injected vaccines, do not activate SIgA. Keep this in mind, it will be important later. 

TRM cells are a special subset of T cells that persist long-term in various mucosal tissues and are not found circulating in our blood. They can kill infected cells, produce cytokines and also have innate-like “sensing and alarming” properties that can recruit other immune cells to control antimicrobial infections. All in all, TRM cells provide immediate and remembered frontline immunity, protecting us against recurrent infections.  

However, not all TRM are created equal. In the skin, TRM remains in the tissue long after infection and antigen clearance. Conversely, lung TRM are lost 4-5 months after an acute infection, leading to the loss of protection from reexposure after this time. 

So this is why, I say again, it seems like the best approach to protect yourself against rapidly mutating respiratory viruses is repeated mucosal exposure in one’s respiratory tract. As this paper notes, 

“Not only is antigen required for TRM formation as previously documented, but unlike the situation in most other organ sites, persistent antigen is essential for the continual replenishment and long-term maintenance of TRM population in the lungs.”. 

In other words, theoretically (as studies specifically on SARS-CoV-2 haven't been performed yet) if you encountered SARS-CoV-2 once, formed TRM cells to the virus and then locked yourself away at home for 5 months alone, you’d lose your TRM cells and become as prone to SARS-CoV-2 reinfection as you did at the start. Who still thinks that lockdowns are a good idea?

Continuous exposure to SARS-CoV-2 and other coronaviruses may help TRM cells to retain memory and prevent reinfection. Don’t take it from me, look at the first line of this study, “Resident memory T cells positioned within the respiratory tract are probably required to limit SARS-CoV-2 spread and COVID-19”. And like SIgA, I must note that vaccines injected into the blood cannot induce TRM cell formation. 

Repeated exposure to respiratory pathogens in short time frames, either naturally or via a respiratory vaccination,  helps to prevent repeated bouts of severe infections. But the trick is not becoming unwell from the virus every time you are exposed to it. 

I believe the key to successfully pulling this off is a particularly strong innate immune system and T cell responses at all times. 

See, viruses are trying to infect us at all times, it is the only way they can replicate. We are surrounded by them. It has been estimated that there are 380 trillion viruses (which is 10 times the number of bacteria) living on and inside your body right now. And an infected human can produce 10^12 infectious viral particles during respiratory virus infection. That’s 10 with 12 zeros after it. 

It has been estimated that we encounter 6 million virus-like particles in the air every day. A teaspoon of seawater typically contains about fifty million viruses. And even in supposedly pristine environments, above the atmospheric boundary layer, the concentrations of viruses have been found to range from 0.26 × 10^9 to >7 × 10^9 m−2 per day.

It is a viral world, and we are simply living in it. Trying to ‘control’ viruses is a futile affair. 

Not only that, but remember that viruses are continuously morphing and selected based on which one survives the thwarting of our immune systems. And so in turn, viruses become more transmissible over time. They also become less deadly we think due to a proposed theory that was formed more than 30 years ago called the ‘virulence-transmissibility evolutionary trade-off’. 

In short, the trade-off hypothesis states that virulence — the harm that a pathogen inflicts on its host through a decrease in host fitness — is an unavoidable cost to the virus for using the host resources for replication. And thus the greater the harm the virus imposes, the greater chance its host (us, in this case) will die and no longer be able to spread to other people and survive. So for transmission to be maximised, intermediate levels of virulence are needed. And though this theory is continuously debated, it seems to hold true for COVID-19.  

So, we’re living in a viral world where their sole aim is to infect us to ensure their survival. As time goes on, our likelihood of viral infection increases, but its threat decreases. Soon SARS-CoV-2 will morph into a form of common cold, we hope. The subtype H1N1 of influenza is a good example of this, still deadly and circulating now, but less so than when it caused the 1918 influenza pandemic, also known as the Spanish flu.

Because there is this persistent and increasing threat of symptomatic infection by SARS-CoV-2, I’d argue that we need to be constantly on guard to prevent this from happening. Remember, the immune system is in flux, and through negative external factors, one can be ‘immune’ one day and not so immune the next. 

It seems like the key to overall respiratory immunity is a strong and well-balanced innate and mucosal T cell response because these are our first-line defences. Only once this level is penetrated do people tend to get symptoms and the formation of antibodies. 

It’s not like the scientific community didn’t know about mucosal immunity. This article titled - “Mucosal Immunity in COVID-19: A Neglected but Critical Aspect of SARS-CoV-2 Infection” was published in November 2020. 

And more recently I was brought to the attention of a May 2022 study on hamsters titled “A live attenuated vaccine confers superior mucosal and systemic immunity to SARS-CoV-2 variants.” In this study, hamsters were either inoculated via their nose with a weakened  SARS-CoV-2 virus or given an injection with an mRNA vaccine. They found that the intranasal vaccine did better on all fronts. They conclude with “Our results demonstrate that use of live-attenuated 10 vaccines may offer advantages over available COVID-19 vaccines, specifically when applied as a booster, and may provide a solution for containment of the COVID-19 pandemic.”.

If mucosal live attenuated vaccines are better than injected mRNA agents, you must ask yourself why so-called 'experts' dismissed the former? Why natural immunity was so vilified? Why lockdowns? Why masks?

Keep questioning.


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