New Study Out Of Sweden Shows Covid Spike Protein From Vaccines Impairs Cell DNA Damage Repair.

a reply to: TheAMEDDDoc

lets see some sources

a reply to: daskakik

or did you just not keep on reading?

Interestingly, the nature of clonal B and T cell responses differed dramatically between infected and vaccinated individuals, suggesting that inflammatory responses associated with infection influence the trajectory of the adaptive immune response – differences that may have important implications for our understanding of durability of protective immune responses.

However, our analysis revealed striking differences in the frequency of key immune populations between COVID-19 patients and healthy volunteers prior to and following vaccination

I've summed up the significant findings of this study. this is the vaxxed as compared to convalescent:

No dramatic upregulation of IFN type I and II

No expansion of  hematopoietic stem and progenitor cells (HSPCs)

No apparent expansion of plasmablasts in circulation following vaccination

Minimal increase in cTfh population

No dramatically elevated cytotoxic signature in NK cells, CD4 and CD8 T cells, and γδ T cells

IGA declines within 7 weeks
-----------------------------------------
Plus you ignored all the other articles I posted.

a reply to: Extremistcontent
But in the end they concluded that the vaccines offer protection despite these differences.

I ignored the rest because none of them backed your claim that NKs and CTLs were being killed off. You harped on this one because of the misinterpretation you gave to that single sentence. So we went with it.

originally posted by: TheAMEDDDoc
a reply to: Extremistcontent

I’m not sure what you are saying? Antibodies are supposed to wane with time, same goes with effector cells. These memory and effector cells are self sustaining and undergo clonal expansion against their targets. You cannot wipe them unless you destroy the progenitor cell populations. You need chemo or radiation or removal of tissue for that.

Neutralizing antibodies have been propped up as the correlate of protection by every single news organization, fauci, Walensky, Gates etc.

Although the presence of antibodies is commonly used as an indicator of protective immunity following vaccination or infection, it may not be the only, nor the key, correlate of immune protection. Indeed, CMI responses are necessary for mounting proper antibody responses in addition to other immune functions. CMI responses to viral infection generally involve different classes of T cells including CD8+ cytotoxic T lymphocytes (CTLs), which kill infected cells, and CD4+ T-helper (Th) cells, which vary by subset in their ability to enhance CTL and antibody responses (Th1 and TFH), modulate immunity at mucosal surfaces (Th17) and regulate these responses and limit tissue damage (Tregs) 4

Monitoring Diversity of COVID-19 Vaccine Induced Immunity Study Investigators: Public Health Agency of Canada/ National HIV & Retrovirology Laboratory:
clinicaltrials.gov...

I'm just making the general statement that no its not antibodies that are the correlate of protection, oh and btw very high levels of antibodies are not good:

Antibodies to SARS-CoV-2 evolve rapidly after infection and coincide with disease progression. Emerging data suggest that early SARS-CoV-2-specific antibody titres are elevated in those with severe disease1, calling into question the role of the antibody response in immunopathology.
previous vaccine studies for SARS-CoV suggest that vaccine-induced antibodies may directly promote enhanced disease upon exposure to the virus

Dissecting antibody-mediated protection against SARS-CoV-2
Tomer Zohar & 
Galit Alter 
Nature Reviews Immunology volume 20, pages392–394(2020)

Oh yeah and whoops it turns out that there are high levels of non-neutralizing antibodies in vacinees, and it was apparent from the early data but we rushed it and nobody noticed, no biggie I'm sure

However, we also found that vaccinees generate more non-neutralizing antibodies than COVID-19 survivors resulting in a lower ratio of neutralizing to binding antibodies.

These data were already apparent in the early phase clinical trials but remained unrecognized at the time
Interestingly, low-titer convalescent serum had the highest relative amount of neutralizing antibodies, whereas the proportion of binding antibodies was increased in sera with higher measured antibody titers.

The majority of plasmablasts sampled after vaccination do, in fact, produce non-neutralizing antibodies.

SARS-CoV-2 mRNA vaccination induces functionally diverse antibodies to NTD, RBD, and S2
Amanat et al. Cell Volume 184, Issue 15, 22 July 2021, Pages 3936-3948.e10
doi.org...

What does it matter anyway, antibodies aren't the correlate of protection...

For non-macrophage tropic respiratory viruses such as RSV and measles, non-neutralizing antibodies have been shown to induce ADE and ERD by forming immune complexes that deposit into airway tissues and activate cytokine and complement pathways, resulting in inflammation, airway obstruction and, in severe cases, leading to acute respiratory distress syndrome10,11,22,23

Both ADE pathways can occur when non-neutralizing antibodies or antibodies at sub-neutralizing levels bind to viral antigens without blocking or clearing infection.

ADE via FcγRIIa-mediated endocytosis into phagocytic cells can be observed in vitro and has been extensively studied for macrophage-tropic viruses, including dengue virus in humans16 and FIPV in cats15.

In this mechanism, non-neutralizing antibodies bind to the viral surface and traffic virions directly to macrophages, which then internalize the virions and become productively infected.

Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies
Nature Microbiology volume 5, pages1185–1191 (2020)

Populations will be central or peripheral, in tissue or circulating. NK and CD8 cell responses will be generated against a viral infection, followed later by antibody generation as support. NK first unless there is a delayed IFN response or the pathogen can produce virokines/viroceptors that trick the NK cell into thinking MHC I and presentation of self is ok in the nucleated cell.

we observed a significant reduction in the production if IFN-α secreted after stimulation with poly I:C and R848 after the administration of the second dose of the vaccine (Figure 1H, 1I). This may hamper the initial innate immune response against the virus, as defects in TLR7 have been shown to result in and increased susceptibility to COVID-19 in young males (Van Der Made et al., 2020).

The BNT162b2 mRNA vaccine against SARS-CoV-2 reprograms both adaptive and innate immune response
PREPRINT
doi: doi.org...

a reply to: daskakik

lol sure.

I've given you many clips from research backing exactly what I've said. Nothing you have said negates any of it.

It must be nice to live in the bliss of ignorance

originally posted by: Extremistcontent
I've given you many clips from research backing exactly what I've said. Nothing you have said negates any of it.

Meh, you moved the goalposts here because you knew everything you had posted didn't back up what you originally said.

how about this, it kills the production of CTL"s and NK's. There. Exact same thing.

Not really the same but you know that.

It must be nice to live in the bliss of ignorance

Beats irrational fear, I guess.

a reply to: daskakik

whats the difference between low NK and CTL's because they aren't produced, and low NK and CTL's because they are killed (a figure of speech, as in killed production)

I can't believe you are still going on about this, well actually yes, its the same tactic of all the uninformed that try to play. Find a little piece of minutae and harp on and on about it.

a reply to: Extremistcontent
None, if they are not needed and what that study shows is that they are not needed to provide protection.

They will be produced if the person becomes infected. That is why we don't go around with huge amounts just circulating all the time. There is a normal range.

Find a little piece of minutae and harp on and on about it.

That is exactly what you did. Find a sentence in a study that is pro-vax and try to say the study was saying the opposite.

a reply to: Extremistcontent

I honestly don’t know where the antibody saves all and prevents infection argument came up. No vaccine prevents pathogen entry and replication but that’s what the media and Fauci say to get people to vaccinate. I don’t get the focus, they don’t just sit around and hang out waiting for the pathogen.

We are always taught, with these types of respiratory viruses, that NK and CD8 T cell function were key with interferon type 1, then type 3 to have the best hope for ISG activation in the host. Then licensing and crosstalk between MHC I and II in dendritic cells and T cells to fill in the gaps. If interferon alpha and beta are delayed, you could die, NK cells won’t keep it in check until cytotoxic T cells respond.

Obesity and diabetes plus age are huge risk factors for a delayed response. In the COVID patients we image for our post mortem ARDS studies, these are what we usually see and vaccination doesn’t matter anymore because interferon is delayed. If I remember right, it’s like 50/50 between groups.

So our target is mediocre at best, it works but not early enough in infection to make a difference. In a perfect world we would have a live attenuated vaccine in the lungs or upper airway that guides the immune system to target some part of the poly protein from ORF1a or maybe ORF1ab and RdRp early in infection. This way, the epithelial cells exposed generate epigenetic changes they pass on to resist infection. Plus you have effector memory T cells locked in tissue that can recruit those in circulation to clear the virus. And the NK cells, DCs, and others get better at recognizing when something is wrong which is a fairly recent discovery. Evidence shows that healthcare workers and those with exposure to other coronaviruses have cross reactive cytotoxic T-cells that wipe the virus early in infection because they targeted these antigens.

With a respiratory virus like this you can’t beat natural infection because your immune response evolves with the virus. We just picked an easy target. I don’t think the vaccines are dangerous or that the virus is either in most. The conspiracy is the money making potential of a vaccine for a”pandemic” that has happened before. The cross reactive T cells with SARS, with other coronaviruses, and from the antibody library were on STAT this or last month, fairly recent and interesting. They also show we may have picked the wrong target and similar viruses have been in circulation before, we just missed it.

If they make a vaccine for the replicase complex then they can’t keep boosting and making money because this could potentially negate all betacoronaviruses, then all coronaviruses, and possibly all RNA viruses that don’t use reverse transcriptase or integrase. The technology is getting close, hopefully they do something about it.

The article does raise questions and the vaccine causes issues in some that produce antibodies to clotting factors or causes some type of issue that activates the alternative or classical pathways of complement, contributing to inflammation and clotting. My only issue is the hyper expression of spike protein in vitro which isn’t natural but great for data collection and proving that the spike can cause issues which they tried to hide for a year or so now. Some people will be very sensitive to its influence. Most will fill in the gaps from the vaccine when exposed to the actual virus.

POST REMOVED BY STAFF

originally posted by: TheAMEDDDoc
a reply to: Extremistcontent

I honestly don’t know where the antibody saves all and prevents infection argument came up. No vaccine prevents pathogen entry and replication but that’s what the media and Fauci say to get people to vaccinate. I don’t get the focus, they don’t just sit around and hang out waiting for the pathogen.

We are always taught, with these types of respiratory viruses, that NK and CD8 T cell function were key with interferon type 1, then type 3 to have the best hope for ISG activation in the host. Then licensing and crosstalk between MHC I and II in dendritic cells and T cells to fill in the gaps. If interferon alpha and beta are delayed, you could die, NK cells won’t keep it in check until cytotoxic T cells respond

Thanks for the reply, I hope this covers much of your reply.

Ineffective IFN innate immunity has been strongly associated with failure to control a primary SARS-CoV-2 infection and a high risk of fatal COVID-19, accompanied by innate cell immunopathology and a plasma cytokine signature of elevated CXCL10, interleukin (IL)-6, and IL-8 in many studies

Sette A, Crotty S. Adaptive immunity to SARS-CoV-2 and COVID-19. Cell. 2021;184(4):861-880. doi:10.1016/j.cell.2021.01.007

These data suggest that a candidate COVID-19 vaccine consisting only of SARS-CoV-2 spike would be capable of eliciting SARS-CoV-2-specific CD4+ T cell responses of similar representation to that of natural COVID-19 disease, but the data also indicate that there are many potential CD4+ T cell targets in SARS-CoV-2, and inclusion of additional SARS-CoV-2 structural antigens such as M and N would better mimic the natural SARS-CoV-2-specific CD4+ T cell response observed in mild to moderate COVID-19 disease.

CD4+ T cell responses were detected in 40%–60% of unexposed individuals.

Regarding the value of cross-reactive T cells, influenza (flu) immunology in relationship to pandemics may be instructive. In the context of the 2009 H1N1 influenza pandemic, preexisting T cell immunity existed in the adult population, which focused on the more conserved internal influenza viral proteins (Greenbaum et al., 2009). The presence of cross-reactive T cells was found to correlate with less severe disease (Sridhar et al., 2013, Wilkinson et al., 2012). The frequent availability of cross-reactive memory T cell responses might have been one factor contributing to the lesser severity of the H1N1 flu pandemic (Hancock et al., 2009). Cross-reactive immunity to influenza strains has been modeled to be a critical influencer of susceptibility to newly emerging, potentially pandemic, influenza strains (Gostic et al., 2016). 

A failure to develop protective immunity could occur due to a T cell and/or antibody response of insufficient magnitude or durability, with the neutralizing antibody response being dependent on the CD4+ T cell response (Crotty, 2019, Zhao et al., 2016). Thus, there is urgent need to understand the magnitude and composition of the human CD4+ and CD8+ T cell responses to SARS-CoV-2. 

SARS-CoV-1 responses, spike was reported as essentially the only target of CD8+ T cell responses (Li et al., 2008),

Our data indicate a somewhat different pattern of immunodominance for SARS-CoV-2 CD8+ T cell reactivity (Figures 6D and 6E), with spike protein accounting for ∼26% of the reactivity, and N accounting for ∼12%. Significant reactivity in COVID-19 recovered subjects was derived from other antigens, such as M (22%), nsp6 (15%), ORF8 (10%), and ORF3a (7%) (Figures 6D and 6E). In unexposed donors, SARS-CoV-2-reactive CD8+ T cells were detected in at least four different donors (Figure S7 ), with less clear targeting of specific SARS-CoV-2 proteins than was observed for CD4+ T cells, suggesting that coronavirus CD8+ T cell cross-reactivity exists but is less widespread than CD4+ T cell cross-reactivity.

The spike protein was a target of human SARS-CoV-2 CD8+ T cell responses, but it is not dominant. SARS-CoV-2 M was just as strongly recognized, and significant reactivity was noted for other antigens, mostly nsp6, ORF3a, and N, which comprised nearly 50% of the total CD8+ T cell response, on average. Thus, these data indicate that candidate COVID-19 vaccines endeavoring to elicit CD8+ T cell responses against the spike protein will be eliciting a relatively narrow CD8+ T cell response compared to the natural CD8+ T cell response observed in mild to moderate COVID-19 disease.

An optimal vaccine CD8+ T cell response to SARS-CoV-2 might benefit from additional class I epitopes, such as the ones derived from the M, nsp6, ORF3a, and/or N.

What I'm looking at here is the shot produces high spike based CD4+ count which is what produces high levels of antibodies which mimics severe disease potentially ADE. This is in comparison to mild or moderate case which is what we want to have happen. Because it is the body's immune reaction to the spike that causes severe disease, and we know that free spike is pathogenic and causes ARDS, stroke, clotting, heart failure etc., there is danger in producing a sever type response. In fact we are seeing that now with all these people "suddenly" dying all over the world, myocarditis rates etc.

Cell. 2020 Jun 25; 181(7): 1489–1501.e15.
Published online 2020 May 20. doi: 10.1016/j.cell.2020.05.015
Target of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals

This is very similar to influenza virus infection, where viral surface hemagglutinin elicited mostly CD4+ T cell responses, whereas the majority of CD8+ T cell responses were specific to viral internal proteins[24]. 

A higher proportion of CD8+ T cell responses was observed in mild disease, suggesting a potential protective role of CD8+ T cell responses in mild disease or a pathogenic role of CD4+ T cell responses in severe disease, which merits further investigation.

The identification of non-spike dominant CD8+ T cell epitopes suggests the potential importance of including non-spike proteins such as NP, M and ORFs in future vaccine designs.

Peng Y, Mentzer AJ, Liu G, et al. Broad and strong memory CD4+ and CD8+ T cells induced by SARS-CoV-2 in UK convalescent individuals following COVID-19. Nat Immunol. 2020;21(11):1336-1345. doi:10.1038/s41590-020-0782-6

a reply to: TheAMEDDDoc

"in individuals with a pre-existing immunity against SARS-CoV-2, the second vaccine dose not only fail to boost humoral immunity but determines a contraction of the spike-specific T cell response.”

"the second vaccination dose appears to exert a detrimental effect in the overall magnitude of the spike-specific humoral response in COVID-19 recovered individuals."

On the other hand, individuals with pre-existing immunity against SARS-CoV-2 should be spared the second dose of the vaccine, at least temporarily, to prevent a possible contraction of their spike-specific memory T cell immunity.

the mechanisms of the contraction of the spike-induced production of IFN-gamma in COVID-19 recovered subjects observed after the second vaccination dose were not investigated. We can only hypothesize that the effector memory CD4+ T cells expanded by first vaccine dose in COVID-19 recovered individuals may be prone to activation-induced cell death (AICD) after the second vaccination dose.

We cannot however exclude that the second dose of the vaccine may only functionally exhaust the spike-specific T cells without really reducing the quantity of the long-term pool of effector memory T cells. Therefore, more detailed analysis of the phenotype of the spike-specific T cells induced by COVID-19 vaccines both in naïve and recovered individuals are needed to answer these questions.

Differential effects of the second SARS-CoV-2 mRNA vaccine dose on T cell immunity in naïve and COVID-19 recovered individuals doi: doi.org...

Despite RT-PCR confirmed COVID-19, specific antibodies to SARS-CoV-2 spike are undetectable in serum in approximately 10% of convalescent patients after mild disease course. This raises the question of induction and persistence of SARS-CoV-2-reactive T cells in these convalescent individuals.

Stimulation with SARS-CoV-2 spike and nucleocapsid (NCAP) as well as HCoV spike peptide pools elicited a similar T cell response in seropositive and seronegative post COVID-19 patients.

Significantly higher frequencies of polyfunctional cytokine nucleocapsid reactive CD4+ T cells (triple positive for IFNγ, TNFα, and IL-2) were observed in both, seropositive (p = 0.008) and seronegative (p = 0.04), COVID-19 convalescent compared to healthy controls and were detectable up to day 162 post RT-PCR positivity in seronegative convalescents. Our data indicate an important role of NCAP-specific T cells for viral control.

Steiner S, Schwarz T, Corman VM, et al. Reactive T Cells in Convalescent COVID-19 Patients With Negative SARS-CoV-2 Antibody Serology. Front Immunol. 2021;12:687449. Published 2021 Jul 12. doi:10.3389/fimmu.2021.687449

Natural infection induced expansion of larger CD8 T cell clones, including distinct clusters likely due to the recognition of a broader set of epitopes presented by the virus not seen in the mRNA vaccine.

Spike specific polyfunctional IFNγ+IL-2+ and IFNγ+TNFα+ CD4, but not CD8, T cells were evident 2 weeks post prime-boost vaccination

CD4 T cells secreted elevated levels of cytokines (IL-6, IL-10), cytotoxic molecules (Granzyme A and Granzyme B), and costimulatory factor (sCD137; soluble 4-1BB) (Figure 3I). Additionally, modest induction of IL-2 and IL-4 by CD4 T cells was measured

Next, we compared the changes in T cell clonal dynamics with infection or vaccination. Vaccination was associated with a shift towards increased CDR3 lengths (Figure 4A). Infection was associated with expansion of large clones (>100 cells), while vaccination induced expansion of primarily small sized clones (2-3 cells)

IL-6 and IL-10 are the two cytokines most associated with severe disease. Notice modest production of IL-2 and IL-4 both are Th2 cytokines. (IL-2 is polyfunctional as it is associated with other Th types, but not Th1). What it looks like is that a very high, strong Th1 response is elicited. Balance is what we want.

More importantly, SARS-CoV-2–reactive T cells in our moderate and severe patients were predominantly of the Th1 phenotype. Although the observed Th1-mediated response is regarded as protective immunity (9, 65), it also can contribute to immunopathogenesis (66). In this context, our finding of a dominant Th2 response of SARS-CoV-2–reactive T cells in mild disease patients raises the question about the beneficial effect of Th1 immunity. One could speculate that even though the Th1 response is generally protective against viral infections, a more balanced combination of Th1/Th2 responses could lead to a milder form of illness among COVID-19 patients. This was illustrated in SARS-CoV-2–responding T cells in patients with mild disease exhibiting a dominant Th2 phenotype (e.g., IL-10, IL-4, and IL-13). It has been shown that COVID-19 infection is more severe in elderly patients with different comorbidities that are generally associated with an inflammatory state and Th1 response (67), whereas children have a tendency to develop an anti-inflammatory Th2 predominant response, which may in part explain a milder course of illness seen after SARS-CoV-2 infection (68, 69). The abundance of IL-4–secreting CD8+ T cells in a group of older adults may not only counterbalance the overproduction of Th1 cytokines but has also been associated with an intact humoral immunity in old age (70). In our study, there was no indication of Th2 response in severe patients but instead a Th17 phenotype was observed. The presence of IL-17+CD8+ T cells in COVID-19 patients with severe disease suggests that these cells may be present in inflamed tissues as reported in the lungs of COPD patients (71).

J Immunol August 15, 2021, 207 (4) 1099-1111; DOI: doi.org...
The Quality of SARS-CoV-2–Specific T Cell Functions Differs in Patients with Mild/Moderate versus Severe Disease, and T Cells Expressing Coinhibitory Receptors Are Highly Activated

Bone marrow plasma cells (BMPCs) are an essential source of medium-term protective antibodies both after vaccination and infection(Halliley et al., 2015; Nutt et al., 2015), but longer-term protection likely requires memory B cells(Iwasaki, 2016; Turner et al., 2021a). Individuals who have recovered from COVID-19 have a significantly lower risk of SARS-CoV-2 reinfection(Hall et al., 2021). A recent 12-month longitudinal study was published with 1,782 plasma samples from 869 convalescent plasma donors in Wuhan, China. This study has shown that among COVID-19 plasma donors the positive rate of IgG antibody against the SARS-CoV-2 receptor binding domain (RBD) in the spike protein exceeded 70% for 12 months post-diagnosis(C. Li et al., 2021). In our study, we show that following vaccination, the levels of anti-SARS-CoV-2 antibodies decrease rapidly, indicating that BMPCs may not be created adequately and therefore anti-SARS-CoV-2 humoral immunity might be transient(Ibarrondo et al., 2020; Seow et al., 2020). After infection, SARS-CoV-2 proteins and nucleic acids could remain in the gut for at least two months, boosting the continued antibody evolution in germinal centers, preferring epitopes overlapping with the ACE2-binding site on the RBD(Gaebler et al., 2021).

SARS-CoV-2 infection induces long-lived bone marrow plasma cells in humans
Version 1. Res Sq. Preprint. 2020 Dec 31.
doi: 10.21203/rs.3.rs-132821/v1

POST REMOVED BY STAFF

a reply to: Smigg

All this has been said by Dr. Geert Bossche for more than a year.
the vaccine is very specific, and is competing against the natural killers created by white blood cells.
This not only opens the door for the infection of new variants it also opens the door for any type of infection.
This means that the first line of defense of the vaccinated is highly compromised, making a mild infection of any kind worse.

LINK
www.geertvandenbossche.org...

check this to
thehighwire.com...
EPISODE 242: THE VANDEN BOSSCHE INTERVIEW

This is so important. It should be front page news. Add to that a Swedish study that says Pfizer's protection is zero after 6 months. What are we doing? Why do we let us being injected like sheeple? Why are the people so gullible about what the media write? When will the realization come? The turnaround?
A new topic on itself but I give you just the link: pfizer: after about 200 days: protection = ZERO
papers.ssrn.com...

POST REMOVED BY STAFF