A recent paper on kidney transplant recipients after COVID vaccination caught my attention because it asked a question that should have been central from the start: what happens at the nasal mucosa, where SARS-CoV-2 first enters the body?
The researchers found that these patients did develop nasal antibodies after vaccination, and some could block the virus from binding ACE2, one of the key steps in infection. But the levels were far lower than in healthy controls.
That detail takes us straight to the problem many people are now living with. They are not asking an abstract scientific question. They are asking, “Why do I keep getting sick?” Repeated respiratory infections, repeated COVID, longer recoveries, and strange symptoms that do not fit the old rules.
The paper matters because it reminds us that protection in the blood is not the same as protection at the border. And for a respiratory virus, the border is the mucosal lining.
The Nose Is Not a Side Issue
When a virus enters through the nose or mouth, it does not start by floating in the bloodstream. It starts by trying to break through the mucosal barrier and infect the cells lining the airway.
This is why mucus matters. When your nose runs with a cold, that is not just an inconvenience. It is defence. The body is trying to trap the virus, dilute it, and move it away before it can attach to cells.
But mucus is more than a mechanical barrier. Embedded in that layer is one of the most important tools we have against respiratory viruses: secretory IgA. It sits in the mucus and binds viruses before they can reach the cells underneath. If it works, the virus is trapped and cleared — coughed out, sneezed out, swallowed, or carried away by normal mucociliary clearance.
This is the first battle. Win it here, and the rest of the immune system may never need to fight.
The Border Patrol Problem
The analogy I keep returning to is border patrol.
Imagine a team is looking for one person, but they have only been trained to recognize a red jacket. If that person arrives in the red jacket, they are caught. But what if they change the jacket, add a hat, put on glasses, or alter their walk?
A poor border patrol misses them. A sophisticated one does not just look for the jacket. It reads height, build, gait, face shape, behaviour — multiple features at once. Even if one changes, the person is still recognized.
That is how broad immunity should work. A narrow response looks only for the red jacket. A broad response looks for the whole person.
This becomes critical with SARS-CoV-2 because the virus changes. If the immune system is trained too narrowly, especially around spike, then changes in spike can blunt recognition. The virus does not need to become invisible. It only needs to become different enough to slip past the first line of defence.
Why Spike Alone Was Never Enough
One of the central mistakes of the pandemic was assuming that a spike-focused systemic response could control a mucosal respiratory virus.
I am not saying injectable vaccines had no role. For high-risk people who had never met the virus, systemic vaccination made sense as a way to reduce severe disease. But if the goal was to reduce infection and transmission, the target should always have been the mucosal lining. That is where the virus enters, where early replication occurs, and where transmission begins.
The Koomen paper shows that vaccination can produce some nasal antibody response. It also exposes the weakness of assuming that a systemic injection automatically builds strong mucosal protection. In immunosuppressed transplant recipients the nasal response was clearly weaker, but the principle is broader: training the immune system in the bloodstream is not the same as training the border patrol at the surface.
That distinction should have been obvious from the beginning.
Koomen, Vera JCH, et al. "Kidney Transplant Recipients Develop Nasal Mucosal Antibodies to SARS‐CoV‐2 With ACE2‐Inhibiting Activity Following mRNA Vaccination." Transplant Infectious Disease (2026): e70230.
The Role of T Cells at the Mucosal Surface
Secretory IgA is only part of the story.
If the virus gets past IgA and infects a cell, the next defence is the T cell response. T cells do not chase free virus. They identify infected cells and destroy them. This matters because once inside, the virus turns that cell into a factory. A single infected cell can produce vast numbers of new particles. Destroy it early, and the infection is contained before it expands.
The way T cells recognize infected cells is remarkable. Viral proteins made inside the cell are processed and displayed on its surface as small fragments — almost like flags. The cell is announcing what is being built inside it.
A broadly trained immune system can read many of those flags. That includes spike, but not only spike: nucleocapsid, membrane and envelope proteins, ORF proteins, non-structural proteins. Natural infection exposes the immune system to a far wider range of viral material than a spike-only approach ever could.
The Difference Between Narrow and Broad Recognition
This is the part I think people need to grasp clearly.
If the immune system is trained mainly to recognize spike, its T cells and antibodies are watching for a limited set of signals. That does not mean there is no response. There is. The question is whether it is broad enough, especially at the mucosal surface, to detect infected cells quickly once the virus changes.
A broader response means multiple T cell populations can recognize multiple viral proteins. That leaves the virus fewer places to hide. Even if one part changes, the others remain visible.
This is why I keep returning to the border patrol. Look for one feature, and the virus has room to evade. Look for many, and it struggles to slip through.
This does not mean every naturally infected person has perfect immunity. They do not. It does not mean every vaccinated person has poor immunity. They do not. Biology is never that simple. But as a general principle, a broad mucosal response should be more resilient than a narrow, spike-dominant one.
Why People May Keep Getting Sick
This is where the discussion becomes uncomfortable.
If the mucosal barrier is weak, the virus crosses the border more easily. Once through, the body has to fight it internally — more inflammation, more tissue involvement, more immune activation, and potentially more cumulative damage.
People may say, “But I did not feel that sick.” That may be true. Yet milder symptoms do not mean a harmless infection. A virus can still drive inflammation, vascular effects, immune disruption and organ stress even when the acute illness seems mild.
This is why repeated infections matter. Each one is not an isolated event. It is another chance for the virus to interact with the immune system, the vasculature, the nervous system, the gut and the airways. If people are being infected again and again, the question is not only why the virus is still circulating. It is why the first line of defence keeps failing to stop it.
The Missed Opportunity
Looking back, the pandemic response should have separated two goals.
The first was reducing severe disease in high-risk people. For that, systemic immune training had a role. The second was reducing infection and transmission. For that, mucosal immunity should have been central.
We never made that distinction clearly enough. We acted as though a systemic vaccine strategy could solve a mucosal transmission problem — always a weak assumption. A more rational approach would have pursued mucosal vaccines far earlier and far harder, studying secretory IgA, nasal T cells, airway immunity, interferon responses and the biology of infection at the portal of entry.
Instead, the public conversation collapsed into antibody levels in the blood. That was never enough.
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Where We Go From Here
We now need honesty.
We need to stop treating repeated infections as normal background noise. We need to stop assuming that mild symptoms mean nothing important has happened. And we need to stop ignoring the mucosal immune system simply because it is harder to measure than serum antibodies.
The future has to be broader. That means looking at secretory IgA, mucosal T cells, gut-airway immunity, nasal nitric oxide, vitamin D status, sleep, metabolic health, chronic inflammation and repeated viral exposure. It means asking why some people are infected again and again while others stay resilient. Most of all, it means moving beyond spike as the whole story.
Spike matters. But it is not the whole virus. And the immune system, properly trained, was never built to watch for one flag. It is built to recognize patterns, multiple signals, and infected cells before the virus takes over.
That is the message I want people to understand. If we are going to explain why so many keep getting sick, we have to look at the border. We have to understand mucosal immunity. And we have to rebuild the kind of broad defence that does not just spot one red jacket, but recognizes the whole threat.
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