The next COVID-19 pandemic clinical presentations will appear confusing without an understanding of the autoimmune nature of the disease.
While scientific opinions may be silenced, predicted outcomes will still occur. Science does not care about politics.
My research has always focused on severe COVID-19 being a viral mediated autoimmune disease. This means the SARS-COV2 viral infection in some persons causes the immune system to recognise specific proteins (serum ACE-2) as being a part of the virus, therefore attacking normal cells with ACE-2, lining blood vessels in the lungs.
McMillan, Philip, et al. "COVID-19—A theory of autoimmunity against ACE-2 explained." Frontiers in Immunology 12 (2021): 582166.
In this review, I aim to delineate some of the patterns that could occur over the next few months.
My great fear is that doing nothing could lead to devastating mortality rates across highly vaccinated regions.
Acute Respiratory COVID-19
This was the typical presentation in the early phase of the pandemic with relatively quick deterioration in respiratory function. Often patients were admitted to hospital requiring oxygen and dependent on the severity could end up in ICU.
Respiratory compromise highlighted by excessive microclots in lung blood vessels was the primary cause of COVID-19 deaths.
These presentations will be reduced as the majority of the population has been exposed to COVID-19 (mucosal immunity) or vaccinated.
Subacute Autoimmune COVID-19
This presentation will be primarily in the vaccinated cohort of the population who do not have adequate mucosal immunity. If the virus causes a systemic response, this could activate an associated autoimmune priming in a small percentage of people.
It is subtle in the symptoms and can mimic many other diseases:
thromboembolic disease through macrophage activation (heart attacks, stroke, peripheral vascular disease)
immune exhaustion in the elderly with secondary bacterial infections
unusual neurologic presentations
progressive frailty and delirium in the elderly
rapid lung deterioration after COVID-19 infection
Post Covid organ dysfunction
Many patients who survived severe COVID-19 will be left with long term organ damage primarily to lungs, heart and kidneys.
The autoimmune priming of their system through infection can be reactivated on subsequent infections. It can only occur if the virus is able to penetrate mucosal defence.
Unless there are associated interferon autoantibodies, the mucosal immunity should remain intact even with further exposure to virus.
It is possible that some of this cohort after vaccination, they can have a spike protein specific immune response instead of the broad mucosal immunity after infection. In this case, they could have an autoimmune reactivation on further exposure to virus.
Prepare for the worst, Hope for the best!
Without an understanding of these patterns, our population will be hit with a tsunami of autoimmune disease over the next few months as variants evade vaccine immunity.
There are options available, but requires current scientific leadership to step back and allow others to lead. Not sure this will happen, and the outcomes could be disastrous.
The description of the problem is rather correct. But the scope of the problem is rather not. This will not be a tsunami, I hope. The hope is based on the following considerations:
- SARS-CoV-2 shall become non-antigenic to vaccinal S-specific memory B and T cell via glycosylation and not be means of protein changes. Epitopes shall remain the same, but the epitopes shall not be reached. There will be limited vaccinal immune response against the new strains of the virus and this shall trigger/require training of innate immunity, that is the only instrument out of endless pandemic.
- vaccinal S-specific memory B cells are long lived plasma blasts not long-lived bone marrow plasma cells. Therefore, vaccinal priming is not irreversible. Post 12-months period after final boost there should be no vaccinal B cells in a majority of vaccinated cohort, I hope. Therfore, ADEI is not life-long risk.
- There should be limited number of non-infected vaccinees. Therefore, even vaccinees have primed immune response (B and T cell) against M, N, E and some nonstructural and accessory proteins, sufficient to avoid autoimmune reactions.
- Phagocytoses, NK cell cytotoxic activity, even vaccinal Abs cytolytic activity all can be sufficient to recognise, neutralize and clear the antigen before it causes adverse effects.
Do not focus so much on threats and weaknesses. Look to strengths and opportunities for objective SWOT analysis of the pandemic. Do not underestimate the innate immunity like vaccinees do. The nature tends to preserve a balance between the pathogen and the host. We shall see, if the host lets the nature to solve the problems its created.
I’ve found your videos very interesting and I’m keeping an open mind - I always like to weigh up all sides.
My personal position is that my fit and healthy wife was fine until she had her second vaccine. She works for the nhs so got them quite early (both Pfizer). As well as working for the nhs she was also a freelance fitness instructor at local gyms teaching mostly body pump and spin, quite often back to back. After the second vaccine she seemed to have overreactions to insect bites, developed shingles, was out of breath to the extent she couldn’t walk a small walk without getting out of breath. She’s currently under the long covid clinic and recently been diagnosed with rheumatoid arthritis. Maybe just coincidental but there do appear to be others with similar issues.
Keep doing your videos - I am disgusted with the way the majority of governments worldwide have treated the public like idiots and not allowed people to choose for themselves. My wife stood to lose her job (at least the threat) if she didn’t get vaccinated. She felt railroaded into getting it and can’t help but think if her health deterioration would have happened if she refused, as do I and the rest of the family.