—>> T Cells <<— (this post is work in progress!)
—> Side topics: viral load, disease tolerance, antibody response, negative efficacy
Negative efficacy of vaccines:
https://drive.google.com/file/d/1zvzgnDxjyTskVkSU9hB45bhDW7f8ljCq/view?usp=drivesdk
Look out for the difference between two studies which compared vaccinated and unvaccinated to the same Omicron variant (B.1.1.529):
Study 1. —> 2X vaccinated, unvaccinated and infection naive (no history of previous infection: first encounter with SARS-CoV-2 was with Omicron !) had T cell response
Study 2. —> 3X vaccinated had ZERO T cell response
How can the immune system become worse despite repeated vaccination (3X) and prior natural infection? There was no immune response in the healthcare workers in this paper from JUN-2022: https://www.science.org/doi/10.1126/science.abq1841
Philip and I had the exact same thoughts on these two points after we read the paper independently.
Has prior immunity induced via natural infection been eliminated? Please note, this post is a work in progress.
I will add more details the next days.
this study shows that some variants can partially escape humoral immunity induced by SARS-CoV-2 infection or BNT162b2 vaccination, but S-specific CD4+ T cell activation is not affected by the mutations in the B.1.1.7 and B.1.351 variants.
https://www.science.org/doi/10.1126/sciimmunol.abj1750
In this study —> Participants vaccinated with Ad26.COV2.S (one or two doses !) or BNT162b2 (two doses !)
South Africa assessed the ability of T cells to react with Omicron spike in vaccinated with Ad26.CoV2.S, BNT162b2, or unvaccinated convalescent COVID-19 patients. 70-80% of the CD4+ and CD8+ T cell response to spike was maintained across study groups.
Here we measured the ability of individuals to cross-recognize Omicron spike following vaccination, prior infection or both. We also studied unvaccinated individuals with no history of previous infection, whose first encounter with spike was with the Omicron variant. We demonstrate that vaccination and infection induce robust CD4+ and CD8+ T cell responses that largely cross-react with Omicron, consistent with recent work from our laboratory and others on limited T cell escape by Beta, Delta and other variants22,23,24. Despite extensive neutralization escape against Omicron5, 70–80% of the T cell response is cross-reactive. In contrast to neutralizing antibody epitopes, T cell epitopes are abundant and located across the entire spike protein20, suggesting that the majority of SARS-CoV-2 spike-specific T cell responses are directed against conserved epitopes and that SARS-CoV-2 viral evasion from T cells may be limited.
SARS-CoV-2-specific CD8+ T cells exhibit the hallmarks of long-lived cells33, and T cell responses to SARS-CoV-1 infection were detectable 17 years later34.
https://www.nature.com/articles/s41586-022-04460-3
Here we studied T cell responses against the structural (nucleocapsid (N) protein) and non-structural (NSP7 and NSP13 of ORF1) regions of SARS-CoV-2 in individuals convalescing from coronavirus disease 2019 (COVID-19) (n = 36). In all of these individuals, we found CD4 and CD8 T cells that recognized multiple regions of the N protein. Next, we showed that patients (n = 23) who recovered from SARS (the disease associated with SARS-CoV infection) possess long-lasting memory T cells that are reactive to the N protein of SARS-CoV 17 years after the outbreak of SARS in 2003; these T cells displayed robust cross-reactivity to the N protein of SARS-CoV-2. We also detected SARS-CoV-2-specific T cells in individuals with no history of SARS, COVID-19 or contact with individuals who had SARS and/or COVID-19 (n = 37). SARS-CoV-2-specific T cells in uninfected donors exhibited a different pattern of immunodominance, and frequently targeted NSP7 and NSP13 as well as the N protein. Epitope characterization of NSP7-specific T cells showed the recognition of protein fragments that are conserved among animal betacoronaviruses but have low homology to ‘common cold’ human-associated coronaviruses. Thus, infection with betacoronaviruses induces multi-specific and long-lasting T cell immunity against the structural N protein. Understanding how pre-existing N- and ORF1-specific T cells that are present in the general population affect the susceptibility to and pathogenesis of SARS-CoV-2 infection is important for the management of the current COVID-19 pandemic.
https://www.nature.com/articles/s41586-020-2550-z
In other words:
https://drive.google.com/file/d/1FJ8IfP2IFgZtuU-p3MWNccc9nzAaeMQQ/view?usp=drivesdk
Survival of infected mice is dependent on CD4+ and CD8+ T cells
We found that the mortality increased to 100% when either CD4+ or CD8+ T cells were depleted.
https://ncbi.nlm.nih.gov/pmc/articles/PMC5201442/
T cell immunity after three vaccine doses:
for S1 B.1.1.529 (Omicron) protein we found a significantly reduced magnitude of response. Overall, more than half (27/50; 54%) made no T cell response against S1 B.1.1.529 (Omicron) protein, irrespective of previous SARS-CoV-2 infection history, compared to 8% (4/50) that made no T cell response against ancestral Wuhan Hu-1 S1 protein (p < 0.0001, Chi-square test) (Fig. 2A). The fold-reduction in geometric mean of T cell response (SFC) against B.1.1.529 (Omicron) S1 compared to ancestral Wuhan Hu-1 S1 protein was 17.3-fold for infection-naïve HCW (blue, p < 0.0001), 7.7-fold for previously Wuhan Hu-1 infected (red, p = 0.001), 8.5-fold for previously B.1.1.7 (Alpha) infected (green, p = 0.002) and 19-fold for previously B.1.617.2 (Delta) infected (purple, p = 0.0625) HCW (Fig. 2B).
T cell and nAb responses against B.1.1.529 (Omicron) were discordant and most (20/27, 74%) HCW with no T cell response against B.1.1.529 (Omicron) S1 made cross-reactive nAb against B.1.1.529 at an IC50 >195 (fig. S4).
We next explored T cell immunity after breakthrough infection during the B.1.1.529 (Omicron) wave. Fourteen weeks after the third dose (9/10, 90%) of triple-vaccinated, previously infection-naïve HCWs showed no cross-reactive T cell immunity against B.1.1.529 (Omicron) S1 protein (Fig. 5A).
Overall, our findings in triple-vaccinated HCW with different previous SARS-CoV-2 infection histories indicated that T cell cross-recognition of B.1.1.529 (Omicron) S1 antigen and peptide pool was significantly reduced.
This paper also shows a low amount of antibodies:
Antibody response has been used to justify vaccine efficacy. However, it is not possible to establish a baseline with antibodies. There were cases where people died with high amounts of antibodies and low. Same for people who survived Covid.
https://www.science.org/doi/10.1126/science.abq1841
You will find an excuse for the failing of the booster due to “immune imprinting” which is not supported by real life data!
Dr Jessica Rose took a look at “immune imprinting”
A new study published in the New England Journal of Medicine (NEJM)* has demonstrated that people who are triple-vaccinated (boosted) against COVID recover significantly more slowly from COVID infection and remain contagious for longer than people who are not vaccinated at all.
The study did not deal with the severity of illness with or without a vaccine.
In other words, people who have received a booster shot are five times more likely still to be contagious at ten days post-infection than are unvaccinated people.
Israeli Health Ministry data shows that in the older population (those over the age of 60), having submitted to more COVID shots often correlates to a greater likelihood of becoming infected with COVID.
https://www.israelnationalnews.com/news/356245
Here we see a negative efficacy no one seems to care about:
https://jamanetwork.com/journals/jama/fullarticle/2792524
Related topics:
Additionally, I wanted to note this take on viral load —» disease tolerance «— Severe disease is not related to viral load.
https://www.pnas.org/doi/10.1073/pnas.2108044118
Viral load —> Comparing unvaccinated vs vaccinated
fully vaccinated individuals with breakthrough infections have peak viral load similar to unvaccinated cases and can efficiently transmit infection in household settings, including to fully vaccinated contacts.
Indication !
Comparing SARS-CoV-2 natural immunity to vaccine-induced immunity: reinfections vs breakthrough infections: SARS-CoV-2-naïve vaccinees had a 13.06-fold increased risk for breakthrough infection with the Delta variant compared to those previously infected.
SARS-CoV-2-naïve vaccinees were also at a greater risk for COVID-19-related-hospitalizations compared to those that were previously infected.
https://www.medrxiv.org/content/10.1101/2021.08.24.21262415v1
—» Besides «—
Imagine they would create a vaccine that gives people all viral targets (structural and nonstructural) orally and not intramuscularly. This might just work 😆 for now:
To claim that vaccines could ever be more effective than
natural infection is illogic and insane -> it's not
possible to create better or the same immunity as
through infections and have it less harmful as infections
<- ZERO chance !!!
I said it from the start: Coronavirus vaccines don’t work for the ones who would need them the most because a functioning immune system is needed to make it work <— That’s the irony of this stupidity they have been trying to sell us.
We encounter endless amounts of pathogens daily. A healthy and fully functioning immune system can handle pathogens as it always has for millions of years.
—> mutation rates of coronaviruses
—> health risk benefit / side effects
—> negative efficacy
END OF STORY !
So why is the push for mRNA vaccines so strong?
Pregnant women were told to be very careful about what they eat. However, mRNA vaccines without long-term safety studies are just fine:
Sources:
Immune boosting by B.1.1.529 (Omicron) depends on previous SARS-CoV-2 exposure
(14 Jun 2022)
https://www.science.org/doi/10.1126/science.abq1841
SARS-CoV-2 variants of concern partially escape humoral but not T cell responses in COVID-19 convalescent donors and vaccine recipients
(28 May 2021)
https://www.science.org/doi/10.1126/sciimmunol.abj1750
T cell responses to SARS-CoV-2 spike cross-recognize Omicron
(31 January 2022)
https://www.nature.com/articles/s41586-022-04460-3
SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls
(15 July 2020)
https://www.nature.com/articles/s41586-020-2550-z
A homolog of the variola virus B22 membrane protein contributes to ectromelia virus pathogenicity in the mouse footpad model
(2016 Nov 26)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5201442/
Variant chasing - it's like trying to dig your way out of a hole. Dig
up, stupid!
(15 JUL 2022)
New study: COVID booster significantly delays end of infection
(Jul 10, 2022)
https://www.israelnationalnews.com/news/356245
Association of Prior BNT162b2 COVID-19 Vaccination With Symptomatic SARS-CoV-2 Infection in Children and Adolescents During Omicron Predominance
(May 13, 2022)
https://jamanetwork.com/journals/jama/fullarticle/2792524
Lessons from a local effort to screen for SARS-CoV-2
(June 17, 2021)
https://www.pnas.org/doi/10.1073/pnas.2108044118
Community transmission and viral load kinetics of the SARS-CoV-2 delta (B.1.617.2) variant in vaccinated and unvaccinated individuals in the UK: a prospective, longitudinal, cohort study
(October 29, 2021)
https://secure.jbs.elsevierhealth.com/action/getSharedSiteSession?redirect=https%3A%2F%2Fwww.thelancet.com%2Fjournals%2Flaninf%2Farticle%2FPIIS1473-3099%2821%2900648-4%2Ffulltext&rc=0
Comparing SARS-CoV-2 natural immunity to vaccine-induced immunity: reinfections versus breakthrough infections
(August 25, 2021)
https://www.medrxiv.org/content/10.1101/2021.08.24.21262415v1
I said it from the start: Coronavirus vaccines don’t work for the ones who would need them the most because a functioning immune system is needed to make it work <— That’s the irony of this stupidity they have been trying to sell us.
We encounter endless amounts of pathogens daily. A healthy and fully functioning immune system can handle pathogens as it always has for millions of years.
—> mutation rates of coronaviruses
—> health risk benefit / side effects
—> negative efficacy
END OF STORY ! ❤️
I suspect it may in part be due to "dampened" TLR 7 & 8 responses, necessary to activate the T cell.
TLR7 [62, 63] Endosome ssRNA viruses (vesicular stomatitis virus, influenza virus)
TLR8 [64–66] Endosome ssRNA from RNA viruses
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7726878/
"In addition, BNT162b2 is nucleoside-modified by a substitution of 1-methyl-pseudouridine for uridine and thus its inherent adjuvant activity mediated by binding to innate immune sensors such as toll-like receptors (TLRs) 7 and 8, is dampened, but not abrogated."
https://www.ema.europa.eu/en/documents/assessment-report/comirnaty-epar-public-assessment-report_en.pdf
comirnaty-epar-public-assessment-report_en.pdf