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. journalofinfection.com/article/S0163-…
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.”
nature.com/articles/s4138…
One more study. While it claims “only” 94 % protection efficacy, the benchmark (PCR+) is much stricter than what was used in vaccine studies (symptomatic infection). The authors report one hospitalization in the previous infection group (could be >99 %).
journalofinfection.com/article/S0163-…
“late asymptomatic RT-PCR re-positivity does occur after COVID-19, even 6 months later, and does not necessarily represent new infection❗️, despite the prolonged time interval elapsed and the negativity of subsequent RT-PCR tests since the first diagnosis”
journalofinfection.com/article/S0163-…
“Our results demonstrate a broad spectrum in the initial SARS-CoV-2-neutralizing antibody response, with sustained antibodies in most individuals for 10 months after mild COVID-19.”
cell.com/cell-host-micr…
Israel: 1st population wide results vaccination vs. infection.
“Vaccination was highly effective with overall estimated efficacy for severe illness 94·4%. …the overall estimated level of protection from prior SARS-CoV-2 infection for severe illness 96·4%” medrxiv.org/content/10.110…
By now, a billion people worldwide have been exposed to the virus and had no or just mild symptoms. They are all immune.
“Seroprevalence due to asymptomatic cases would be equivalent to that of general population.”
medrxiv.org/content/10.110…
Some asymptomatic individuals mount more robust immune responses than symptomatics.
“Our study shows that healthy individuals can mount robust immune responses against SARS-CoV-2 without symptoms.”
cell.com/iscience/fullt… Image
“antibody reactivity to the receptor binding domain (RBD) of SARS-CoV-2, neutralizing activity and the number of RBD-specific memory B cells remain relatively stable from 6 to 12 months.”
Also, natural immunity covers variants of concern.
biorxiv.org/content/10.110…
Zero reinfection identified among previously infected and 4 reinfections among (three times as many) vaccinated young people (median age: 29 years).
medrxiv.org/content/10.110…

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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? sciencedirect.com/science/articl…
Reviewed here:
Potential adverse effects of nanoparticles on the reproductive system
dovepress.com/potential-adve…
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,
science.sciencemag.org/content/early/…
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
28 Apr
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/
bmj.com/content/372/bm…
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/
Read 22 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).
nature.com/articles/d4158… 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.
frontiersin.org/articles/10.33…
An excellent bird’s view of the same topic.
cell.com/cell-systems/f…
Read 12 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”
pnas.org/content/117/41… 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
👇🏻👇🏻👇🏻
journals.sagepub.com/doi/10.1177/17…
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. imperial.ac.uk/news/207333/co…
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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