There’s a curious correlation between countries/regions of high prior SARS2 exposure and a resurgence upon the start of mass V immunization programs. I’ve been thinking a lot about this lately, and the only explanation that could fit observations is… 1/…
reactivation of dormant viruses in the population. (Seasonal) respiratory viral dormancy has been debated a lot for decades, but there’s still no consensus on where exactly these virions could lay dormant in the body, nor on the trigger(s) & mechanism(s) responsible for… 2/
reactivation. In light of recent research, my (educated?) guess is that the small intestine, and associated immune structures, is more likely place for this to occur than the respiratory tract. Admittedly, this is speculative, but neither implausible nor could I come up with… 3/
an explanation that better fits what’s seen in more and more countries.
Initially, I thought that poorly organized vaccination campaigns and careless behavior of vaccinated might explain the phenomenon, but it’s been becoming clear that this cannot be the case.
I’ll keep amending this mini-thread with (potentially) supporting evidence.
Just as infection with other viruses, vaccination can also reactivate e.g. shingles.…
Immunosuppressive states are also known to result in reactivation of dormant viruses. Space travel is one such example. The week (or so) following a strongly immunogenic systemic vaccination is also immunosuppressive.…
Adding this case report here. Thanks for sharing.
Evidence for viral dormancy at least up to 6 months.
I forgot about one of the most obvious examples of (transient) immunosuppression: irradiation. Note the time span of 1-2 weeks.…
These findings may support the case.
Longitudinal following a lot of cats showed that feline coronavirus can establish chronic infection and perhaps dormancy with periodic deactivation as well. (No sequencing was done to confirm.)…
Look at this, population data from Denmark.
“Suspected COVID-19 cases that occurred within 7 days after any vaccination were 409 in the vaccine group vs. 287 in the placebo group.”
Largest collection of real world examples I’ve seen so far.
The phenomenon described in Ebola as well.
Now, this is really intriguing. Image
The discrepancy in below data from Israel suggests the same. Cases and deaths increase during the ~2-week period following the first vaccination. I find it a bit weird that the authors decided not to report on this part at all.
Here you go. Both antigen (S1) and viral RNA is confirmed >12 months in monocytes derived from survivors of severe COVID and ‘long COVID’. Hopefully the authors will map other antigen presenting cells and various tissue localization in the future.…
Similarly intriguing development in Uruguay.
“Almost half of Kenyan adult donors had evidence of past SARS-CoV-2 infection by March 2021.
***Between March and June, 2% of the population were vaccinated against COVID-19 and the country experienced a third epidemic wave***.”
Emphasis mine…
Look how this has been going.… Image
Long COVID is correlated with EBV reactivation. Some people describe ‘long vaccine’ as well. Intriguing…

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More from @gerdosi

22 Jun
Once again, old science (image to the left) predicts new findings (image to the right). One thing remains common: negligence

Accumulation of nanocarriers in the ovary: A neglected toxicity risk?…
Reviewed here:
Potential adverse effects of nanoparticles on the reproductive system…
The literature is full of papers that describe lipid nanoparticles as specific delivery machines of (e.g. anti-cancer) drugs to the ovaries.
Read 4 tweets
11 May
1/ I have a thread about natural immunity to SARS-CoV-2, but I was asked to do a comparison with vaccine induced immunization. Interestingly, deep analysis of the two is largely missing. A recent study will do the job,…
2/ but we need to focus on results, not conclusions, because even though the study was designed to compare the two types of immunization, plus added the effect of a booster jab on top of infection, the interpretation is a bit twisted to mostly compare the 2 jab scenarios.
3/ Quote:
"Three individuals who previously showed a response, despite lack of laboratory evidence for infection (therefore presumably a cross-reactive response to an endemic human coronavirus) showed an unchanged or decreased [T cell] response to spike after vaccination."
Read 32 tweets
20 Jan
The autoimmunity problem raised by below article requires rethinking of pathophysiology and treatment of severe COVID-19. The level of mimicry between spike and human peptides is very high (see attached figure from a researcher featured in the article).… Image
Unfortunately, this seems more than theoretical matches.
“SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues” & more.…
An excellent bird’s view of the same topic.…
Read 12 tweets
28 Dec 20
New mRNA vaccine technologies may offer 94-95 % efficacy. What an achievement of 21st century science!
On the other hand, good old natural immunity provides 100 % protection from symptomatic COVID-19, as shown in the study of 12.5k healthcare workers below.
Another large study finds precisely the same thing: 100 % natural immune protection from symptomatic COVID-19 within 6 months of first infection.…
What could provide lasting protection? Repeated exposure.
Tissue resident memory T cell presence “required airway vaccination and antigen persistence in the lung, as non-respiratory routes of vaccination failed to support long-term lung TRM maintenance.”…
Read 11 tweets
13 Dec 20
What a coincidence
“The binding epitope on S harbors a sequence motif unique to SARS-CoV-2 (not present in other SARS-related coronaviruses), which is highly similar in both sequence and structure to the bacterial superantigen staphylococcal enterotoxin B”… Image
Now, this story keeps unfolding.
“the trimeric spike protein of SARS-CoV-2 could bind to TLR4 directly and robustly activate downstream signaling in monocytes and neutrophils.” Via MyD88 and NFκB
See how MyD88 activation is THE problematic pathway, especially when amplified by elevated LPS exposure. I.e. by metabolic diseases.
How the two pathways join at this signaling node
Read 22 tweets
27 Oct 20
1/ Thread on immunity in the respiratory system: how it does and doesn't work (i.e. myths), simplified as much as I could. I’ll use the apropos of a new press release by Imperial College. To avoid mainstream media fantasies, let's use the original piece.…
2/ The main pillars of mucosal immunity in the respiratory system are:
– Innate immunity. This ancient part includes the physical barrier: mucus production and continuous flow upwards, driven by ciliary epithelial cells. There are also phagocytes ("eating cells") and…
3/ …other cellular components that produce signaling molecules, set traps, etc.

– Adaptive immunity
---> B & plasma cells that release antibodies into the airways through the single cell layer called the epithelium.
Read 21 tweets

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