Spike proteins

UKHSA says that Infection-Acquired N-Antibodies are Lower in the Jabbed

Is this a big deal? It might be.

Thanks go to Alex Berenson, banned from Twitter, for bringing this information to light.

Alex thinks it is a big deal:

Take it from a little place I call the British government. Which admitted today, in its newest vaccine surveillance report, that:

“N antibody levels appear to be lower in people who acquire infection following two doses of vaccination.” (Page 23)

What’s this mean? Several things, all bad. We know the vaccines do not stop infection or transmission of the virus (in fact, the report shows elsewhere that vaccinated adults are now being infected at much HIGHER rates than the unvaccinated).

What the British are saying is they are now finding the vaccine interferes with your body’s innate ability after infection to produce antibodies against not just the spike protein but other pieces of the virus. Specifically, vaccinated people don’t seem to be producing antibodies to the nucleocapsid protein, the shell of the virus, which are a crucial part of the response in unvaccinated people.

This means vaccinated people will be far more vulnerable to mutations in the spike protein EVEN AFTER THEY HAVE BEEN INFECTED AND RECOVERED ONCE (or more than once, probably).

It also means the virus is likely to select for mutations that go in exactly that direction, because those will essentially give it an enormous vulnerable population to infect. And it probably is still more evidence the vaccines may interfere with the development of robust long-term immunity post-infection.

Aside from that, everything is fine.

Alex might be right about these things. From the paucity of the information provided from UKHSA Report 42, it’s not immediately obvious, but it’s certainly concerning.

So, as usual, in order to try to get a clearer picture of what this might mean, I go to the source. The seroprevalence data comes from blood donors and they measure levels of S (spike) antibodies and N (nucleocapsid) antibodies.

The results presented here are based on testing samples with Roche nucleoprotein (N) and Roche spike (S) antibody assays. Nucleoprotein (Roche N) assays only detect post-infection antibodies, whereas spike (Roche S) assays will detect both post-infection antibodies and vaccine-induced antibodies. Thus, changes in seropositivity for the Roche N assay reflect the effect of natural infection. Increases in seropositivity as measured by S antibody reflect both infection and vaccination.

That seems to be fairly clear. Level of N-antibodies exclusively record exposure to natural infection whereas S antibody levels record both natural exposure to the virus and immunisation and apparently, it’s impossible to discriminate which is which. So the presence of N-type antibodies is our only reliable guide to exposure to the wild virus. What we don’t know is what constitutes an ‘infection’, whether the presence (or not) of antibodies is a reliable guide to an actual, symptomatic infection whereby the person infected becomes a potential transmitter because of the presence of an actively replicating virus coupled with a sufficiently high viral load present in the nasal cavities. With high viral load, double-jabbed pre or even asymptomatic superspreaders of delta now being a thing, the picture gets complicated. Here is what the report authors say about national prevalence:

Overall population weighted (by age group, sex and NHS region) antibody prevalence among blood donors aged 17 years and older in England was 18.7% (95% CI 17.7% to 19.8%) using the Roche N assay and 98.0% (95% CI 97.7% to 98.3%) using the Roche S assay for the period 16 August to 10 October (weeks 33 to 40 2021). 1,334 out of 7,384 were Roche N positive and 14,815 out of 15,081 samples were Roche S positive. This compares with 14.9% (95% CI 14.1% to 15.8%) Roche N seropositivity and 92.3% (95% CI 91.9% to 92.7%) Roche S seropositivity for the period of 24 May to 13 August 2021 (weeks 21 to 32 2021).

Here are two of the graphs for prevalence:

What is immediately clear is that the sharp rise in spike antibodies is almost certainly related to the vaccine rollout beginning in December 2020. The rise in N-Abs is much more gradual and is probably a reflection of gradually increasing prevalence, especially in the younger age groups, who are far less likely to suffer from noticeable symptomatic infections, but may nevertheless contract a very mild form of the virus, enough for their immune systems to generate antibodies against the virus shell. This suggests that the prevalence of the SARS-CoV-2 virus has been increasing, but not at an alarming rate, although there has been a fairly sustained increase in natural infections in people under 40 since about week 23. Here is what the authors have to say about the Roche antibody level serum tests in blood donors:

Roche S seropositivity in blood donors has plateaued and is now over 96% across all age groups. Seropositivity estimates for S antibody in blood donors are likely to be higher than would be expected in the general population and this probably reflects the fact that donors are more likely to be vaccinated. Seropositivity estimates for N antibody will underestimate the proportion of the population previously infected due to (i) blood donors are potentially less likely to be exposed to natural infection than age matched individuals in the general population (ii) waning of the N antibody response over time and (iii) recent observations from UK Health Security Agency (UKHSA) surveillance data that N antibody levels appear to be lower in individuals who acquire infection following 2 doses of vaccination.
Vaccination has made an important contribution to the overall Roche S increases observed since the roll out of the vaccination programme, initially amongst individuals aged 50 years and above who were prioritised for vaccination as part of the phase 1 programme and more recently in younger adults as part of phase 2 of the vaccination programme.

They suggest that N antibody seropositivity is probably an underestimate because:

(i) blood donors are potentially less likely to be exposed to natural infection than age matched individuals in the general population

(ii) waning of the N antibody response over time

(iii) recent observations from UK Health Security Agency (UKHSA) surveillance data that N antibody levels appear to be lower in individuals who acquire infection following 2 doses of vaccination.

I can’t think why (i) might be an issue. With regards to (ii), antibody levels do definitely wane over time after exposure so this might mean that the shape of the curves above is correct, but they should be shifted up a few percent. But (iii) is a bit of a concern. It seems to suggest that with so many now double-jabbed, exposure to the wild virus is eliciting a more muted N-antibody response in those who have been double-jabbed (the majority of adults) compared to those who have resisted the government’s extreme coercion tactics thus far. As N antibody levels are a measure of natural adaptive immunity following exposure to the whole live virus, this might present a serious concern. Will Jones at the Daily Sceptic thinks it could be evidence of Original Antigenic Sin, which I’ve discussed previously.

A further thing revealed for the first time in this week’s surveillance report is that the vaccines may actually hobble the body’s ability to develop the strongest immunity once infected. As noted by Alex Berenson, the report mentions (in passing) that “recent observations from UK Health Security Agency (UKHSA) surveillance data” show that “N antibody levels appear to be lower in individuals who acquire infection following two doses of vaccination”.

There is no elaboration on this, but on the face of it it is a startling admission. It is basically saying that a certain kind of antibody which is not produced by the vaccines but is usually produced by infection (and hence is used by PHE/UKHSA to identify those with antibodies-from-infection) is not produced so well by those who are infected post-vaccination. Insofar as this is true it means the vaccines may actually prevent the immune system from developing the strongest form of protection against reinfection. This phenomenon of the immune system being in some way hobbled by the way it first encounters a pathogen is well-known and is referred to as original antigenic sin.

It might be OAS, but I understood that to be the inability of the immune system to respond effectively to a new variant. So, in the case of the S-directed antibody response elicited by the vaccines, when the vaccinee is exposed to a virus with a significantly changed spike protein, the S-immune response ‘remembered’ by the trained immune system, will not be sufficient to neutralise the new spike antigen, hence the viral variant will be able to ‘escape’ vaccine immunity. What we seem to have with the nucleocapsid protein immune response – unique to natural infection – is that it is being diminished somehow because of vaccination. If that’s the case, it’s not good, not good at all. Why? Because mutated spike variants of the SARS-CoV-2 virus undermine the vaccine immune response (based on obsolete spike versions), but in addition to this, the broad spectrum natural immune response (which is much less affected by mutations in the spike) is also being compromised, which means that double and triple-jabbed people may be in for a very bumpy ride if they come into contact with increasingly more altered spike versions of the SARS-CoV-2 virus.

The importance of the nucleocapsid immune response is outlined below:

The accompanying text explains:

If we group vaccine antibody responses against natural infections, then we see a clear difference (Figure 2).

The data indicates a greater than 2 log increase in nucleocapsid IgG antibody signal after natural infection (median log2 MFI = 8.45) compared to pre-exposure or post-vaccination antibody levels (median log2 MFI = 6.38 and 6.36, respectively).

The following graph shows quite clearly that whereas natural infection elicits both S and N antibodies, vaccination only stimulates S-antibodies and indeed, the J&J vaccine appears to diminish the production of N-type antibodies.

This is further exemplified here:

Figure 3. Antibody signatures against full length SARS-CoV-2 proteins and subunit peptides following vaccination or natural infection. Each participant’s pre-vaccine or infection value was subtracted from their post value for each protein or peptide. Cohort values were averaged. Each row indicates a unique peptide or protein. The greater the difference, the more red the color. Blue indicates a decline in antibody binding after the immune event. Values are on Log2 scale. Chart is interactive, use the filter at the top to select specific proteins or peptides to view.

Note that the vaccines, after injection, tend to produce a decline in antibody binding to the nucleocapsid region.

Nucleocapsid is a protein involved in genome packaging and viral assembly. It is not found on the surface of SARS-CoV-2.

S, however, is found on the virus surface, which is the reason it is the dominant immune target after infection.

Due to the greater immune pressure it receives, S protein mutates more rapidly than nucleocapsid. When variants are discussed, the implied variation is in the S protein.

The reduced immune pressure on nucleocapsid helps conserve its sequence and structure, which could mean nucleocapsid antibodies retain effectiveness against emerging SARS-CoV-2 variants.

This explains why it is vitally important to preserve N-antibody response and why infection acquired immunity is more robust than narrow spectrum spike-directed vaccine immunity.

Revealed: Why the Oxford AstraZeneca Jab is Even More Dangerous than the mRNA ‘Vaccines’

People are dying and suffering from serious illness, including strokes, brain haemorrhages, blood clotting, blindness, heart attacks, neurological/nervous disorders, etc. soon after getting jabbed with any of the ‘vaccines’ currently available in the UK – Pfizer, Moderna and Oxford/AstraZeneca. This is a fact. 44 year old BBC presenter Lisa Shaw has just died from a blood clot, having been injected with AZ’s viral vector ‘vaccine’ – as part of a scandalously coerced mass vaccination program, in violation of the Nuremberg Code, fully supported by and sold to a gullible, fearful public by her own employer. The AZ jab definitely appears to be – at present – the worst offender as far as serious adverse reactions are concerned.

Our government, the media, the NHS and the MHRA tell us that this carnage means the AZ jab is ‘safe and rigorously tested’. 182,751 people, including 806 dead people, might disagree. Let us also be aware that many adverse reactions are not being reported, and indeed there is evidence to suggest that doctors and medical staff are deliberately not reporting adverse reactions to the jabs in those people they coerced to get jabbed. The VAERS database in the US for instance, is cited as recording only 1-10% of all adverse drug reactions.

Considering that many of the victims of this mass stabbing exercise by the state are people who are at minimal risk from Covid, considering that many of them will have already had robust and durable natural immunity to Covid anyway, via past infection, this is a massive scandal and evidence of an ongoing crime against humanity.

We now have emerging research which might explain why the adenovirus vectored Oxford AZ DNA jab is even more dangerous than the mRNA Pfizer and Moderna jabs. It has to do with the genetically modified chimpanzee adenovirus itself and the way in which it gets its ‘payload’ of SARS-Cov-2 spike encoding DNA into our cells.

During the last months many countries have started the immunization of millions of people by using
vector-based vaccines. Unfortunately, severe side effects became overt during these vaccination
campaigns: cerebral venous sinus thromboses (CVST), absolutely rare under normal life conditions, were
found as a severe side effect that occured 4-14 days after first vaccinations. Besides CVST, Splanchnic
Vein Thrombosis (SVT) was also observed. This type of adverse event has not been observed in the
clinical studies of AstraZeneca, and therefore led immediately to a halt in vaccinations in several
european countries. These events were mostly associated with thrombocytopenia, and thus, similar to the
well-known Heparin-induced thrombo cytopenia (HIT). Meanwhile, scientists have proposed a mechanism
to explain this vaccine-induced thrombocytopenia. However, they do not provide a satisfactory
explanation for the late thromboembolic events. Here, we present data that may explain these severe side
effects which have been attributed to adenoviral vaccines.

What is the fundamental difference between mRNA and vector-based vaccines? The mRNA vaccines are
delivered by a lipid nanoparticle containing the appropriate mRNA molecule – coding for the spike protein
of SARS-CoV-2 – to muscle cells surrounding the injection site. Cells that have successfully taken up these
nanoparticles will release their cargo mRNA into the cytosol, where it will be translated into Spike protein
in the rough endoplasmatic reticulum (ER). Subsequently, the translated and folded Spike proteins will be
post-translationally modified in the ER and Golgi apparatus and transported to the outer membrane – as
membrane-anchored proteins. This way, the immune system is able to recognize the viral antigen, which
in turn triggers the initial events for all subsequent immunological processes to produce specific B- and T effector cells.
What happens to the same Spike gene when delivered via an adenoviral system? The adenovirus life
cycle includes the infection of cells, uncoating of the virus in the cytosol, entry of the adenoviral DNA into
the nucleus, and subsequently gene transcription by the host transcription machinery (6). All adenoviral
systems follow exactly these steps (Ad5, Ad26 and chimp Ad). Thus, the SARS-CoV-2 Spike gene will be
transcribed inside of the nucleus and subsequently exported as mRNA out of the nucleus. Arriving in the
cytosol, the mRNA will again be translated into the Spike protein (see above).
And exactly here lies the problem: the viral piece of DNA – deriving from an RNA virus – is not optimized to
be transcribed inside of the nucleus. Solely this 3,822 nucleotide long open reading frame, coding for a
primary product of 1274 amino acid long Spike protein, contains 6 predicted splice donor and 5 predicted
acceptor sites. This problem becomes even more severe when using codon-optimized Spike reading
frames (depending on the company: up to 13 splice donor and 11 acceptor sites; see Fig. 1A). Thus, it
could well be that the Spike open reading frame of SARS-CoV-2 is potentially disrupted by arbitrary splice
events when transcribed inside the nucleus. Most, if not all, of these undesirable splice events would
produce shorter protein variants, disrupting the Spike protein upstream of the C-terminally located
membrane anchor, and thus, leading to soluble Spike protein variants.

In simple translation, what the authors are saying here is that because the AZ and other ‘vaccines’ deliver a piece of DNA (not mRNA) directly into the cell nucleus via the adenovirus vector, then there is the possibility that errors will occur when that DNA is transcribed back into RNA inside the nucleus. Thus, when the RNA is expelled from the nucleus into the surrounding cell material and starts instructing the cell machinery to manufacture the SARS-CoV-2 spike protein, those spike proteins produced might be ‘missing bits’; they will be shorter versions of the actual spike protein which, as result, will be able to migrate into the blood vessels where they will bind to platelets and cause serious health issues, namely haemorrhaging and clotting, which is exactly what we are seeing with AZ adverse reactions.

It’s not just the AZ ‘vaccine’:

The authors give the mRNA ‘vaccines’ a free pass on safety because they say that this production of soluble spike proteins just can’t happen with mRNA delivered into the cell cytosol:

Here, we present first molecular evidence that vector-based vaccines encoding the Spike protein exhibit a
problem that is completely absent in mRNA-based vaccines. This is due to the fact that during the
vaccination step, the adenoviral DNA enters the nucleus and use the host machinery to transcribe its
(trans)genes inside the nucleus. However, RNA viruses have evolved in the absence of any post transcriptional modifcation systems that are usually enabled to process the primary RNA transcripts of
nuclear encoded genes.

They even say the AZ ‘vaccine’ can be ‘re-optimized’:

Based on our findings, we strongly suggest that the Spike open reading frames – wildtype or codonoptimized in vector-based vaccines has to be re-optimized to avoid unintended splice reactions and to increase the safety of these pharmaceutical products. Vice versa, all mRNA-based vaccines should represent safe products, because the delivered mRNA will only be translated into surface antigen, without having any possibility to participate in nuclear splice events.

Unfortunately, spike proteins ‘leaking’ into the blood system can and do happen with other type ‘vaccines’ also, so it’s not a problem unique to AstraZeneca. The mRNA ‘vaccines’, though apparently less dangerous than the Oxford AZ viral vector vaccine, still have a whole host of serious side effects including thrombotic events like clots, strokes, heart attacks, haemorrhages, many linked to thrombocytopenia (low blood platelet count). Something which the manufacturers said couldn’t happen, has happened: spike proteins have been detected circulating in the blood of several volunteers who were administered the Moderna ‘vaccine’. Supposedly, they are at such minute concentrations that they cannot cause damage, but then this underpowered study looked at just a handful of healthy volunteers who were not suffering serious adverse side effects. The point is, the ‘experts’ have no explanation as to why they are there at all.

SARS-CoV-2 proteins were measured in longitudinal plasma samples collected from 13 participants who received two doses of mRNA-1273 vaccine. 11 of 13 participants showed detectable levels of SARS-CoV-2 protein as early as day one after first vaccine injection.

Nonetheless, evidence of systemic detection of spike and S1 protein production from the mRNA-1273 vaccine is significant and has not yet been described in any vaccine study, likely due to limitations in assay sensitivity and timing assessment. The clinical relevance of this finding is unknown and should be further explored.

It’s not just soluble SARS-CoV-2 spike proteins

The Daily Fail would have us believe that the problem with the AZ ‘vaccine’, which is just ‘very rare’ brain haemorrhages, has now been identified and can be fixed. Not really a big deal according to them.

Germans scientists say they have figured out why the Covid vaccines from  AstraZeneca and Johnson & Johnson are linked to rare blood clots

In a new pre-print, the team says the problem is with the adenovirus vector, a common cold virus used to get the body to induce an immune response

They claim the vaccine is sent into the cell nucleus instead of surrounding fluid, where parts of it break off and create mutated versions of themselves 

The mutated versions then enter the body and trigger the rare blood clots

Scientists say they can genetically adapt the vaccine to prevent the virus’s spike proteins, which it uses to enter cells, from splitting apart

That’s all OK then. What they don’t tell you, probably because they didn’t read the study carefully, assuming they even read it at all, is that this newly identified faulty transcription of DNA to RNA, resulting in the production of truncated, soluble spike proteins, is not the only problem with the viral vector ‘vaccines’. The other major problem is the genetically modified adenovirus vector itself. It too can bind to platelets and cause thrombocytopenia. The issue has been known about for at least 15 years, so there’s no excuse for the manufacturers to claim that such an adverse effect was unforeseen – it wasn’t. Here for instance:

Thrombocytopenia has been consistently reported following the administration of adenoviral gene transfer vectors. The mechanism underlying this phenomenon is currently unknown.

And here:

Thrombocytopenia is a major adverse effect of high dose systemic administration of adenoviral (Ad) gene therapy vectors. While a previous report did not find platelet activation by Ad [1], recent studies have shown that Ad may activate platelets [2] and binds in vivo to murine thrombocytes resulting in hepatic sequestration [3]. Ad-induced thrombocytopenia has been shown to be dose-dependent, saturable and reversible [4], compatible with a ligand-receptor mechanism. Recently, binding of Ad to platelet was indirectly suggested following interference of platelet adhesion to fibronectin after incubation with Ad [2]. In this study we developed a direct flow cytometry assay to quantitatively analyze Ad attachment to human platelets in vitro and to characterize their interaction.

What this clearly tells us is that there are two major problems with the AZ viral vector vaccine, giving rise to very similar serious thrombotic adverse reactions associated with a low blood platelet count and those two problems arise separately as a result of SARS-CoV-2 spike proteins migrating into the blood, plus the adenovirus itself binding to blood platelets. The authors of this new study do actually point this out, but then they appear to ignore it, along with the media reporting on the paper.

Therefore, we propose a pathological disease mechanism that is depicted in Fig. 1D. On one hand, the
recently described VITT mechanism
is based on the artificial activation of PF4 by adenoviral proteins or
DNA molecules, which can similarly to heparin, act as a poly-anion to mediate PF4 activation. In patients
that exhibit a high load of auto-antibodies against PF4, this may cause the observed thrombocytopenia
(Fig. 1D, left side). The other side of the pathological disease mechanism is depicted as well (Fig. 1D, right
side). Based on our splicing data, membrane-anchored and soluble Spike protein variants are produced
after the vaccination procedure. When the immune system now starts the production of anti-Spike
antibodies (days 4–16), these antibodies will recognize the membrane-anchored as well as soluble Spike

VITT is Vaccine Induced Thrombosis and Thrombocytopenia and is a known adverse effect of adenovirus gene therapy vectors, not just ‘vaccines’. Drug companies have known about the dangers for years. Here is the handy diagram provided by the authors of the new study, which distinguishes between the two:

In summary, the AZ ‘vaccine’ is dangerous; (a) as a result of a known side effect of the administration of adenovirus vectors, (b) as a result of an unforeseen faulty transcription of DNA into RNA, resulting in the production of soluble spike proteins, which are binding to blood platelets. The mRNA vaccines appear not to be so dangerous, but they certainly don’t have a free pass on safety, as implied wrongly by the authors of the new study on AZ adverse reactions.

Salk Institute: SARS-CoV-2 Spike Proteins Cause Damage To Blood Vessels But the Same Spike Proteins Coded By the Vaccines Are Safe!

We already knew that the SARS-CoV-2 spike proteins were implicated in serious damage to blood vessels in severe cases of Covid disease in the immune-compromised. Here (Sept 2020) for instance:

Critically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk.

We demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo.

Our findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.

Or here (Jan 2021):

It was found that the treatment of cultured primary human pulmonary artery smooth muscle cells (SMCs) or human pulmonary artery endothelial cells with the recombinant SARS-CoV-2 spike protein S1 subunit is sufficient to promote cell signaling without the rest of the viral components [21]. Furthermore, our analysis of the postmortem lung tissues of patients who died of COVID-19 has determined that these patients exhibited pulmonary vascular wall thickening, a hallmark of pulmonary arterial hypertension (PAH) [21]. Based on these results, we proposed that the SARS-CoV-2 spike protein (without the rest of the viral components) triggers cell signaling events that may promote pulmonary vascular remodeling and PAH as well as possibly other cardiovascular complications [21,22].

The Salk Institute have recently published another study which comes to much the same conclusions. They seem to think they might be the first to discover the mechanism whereby the spike causes endothelial damage:

The paper, published on April 30, 2021, in Circulation Research, also shows conclusively that COVID-19 is a vascular disease, demonstrating exactly how the SARS-CoV-2 virus damages and attacks the vascular system on a cellular level. The findings help explain COVID-19’s wide variety of seemingly unconnected complications, and could open the door for new research into more effective therapies.

“A lot of people think of it as a respiratory disease, but it’s really a vascular disease,” says Assistant Research Professor Uri Manor, who is co-senior author of the study. “That could explain why some people have strokes, and why some people have issues in other parts of the body. The commonality between them is that they all have vascular underpinnings.”

While the findings themselves aren’t entirely a surprise, the paper provides clear confirmation and a detailed explanation of the mechanism through which the protein damages vascular cells for the first time. There’s been a growing consensus that SARS-CoV-2 affects the vascular system, but exactly how it did so was not understood. Similarly, scientists studying other coronaviruses have long suspected that the spike protein contributed to damaging vascular endothelial cells, but this is the first time the process has been documented.

Previous studies have shown a similar effect when cells were exposed to the SARS-CoV-2 virus, but this is the first study to show that the damage occurs when cells are exposed to the spike protein on its own.

Just looking at the other two studies cited above (which are by no means exhaustive) I think Salk’s claim to originality is somewhat dubious. But what is even more dubious is their claim (minus any proper scientific evidence) that the spike protein of the virus itself can cause serious cardiovascular symptoms independent of the virus in those infected with SARS-CoV-2 but that, for some mysterious reason, the very same spike proteins generated by the body’s cells after vaccination are ‘safe’ and do not cause such symptoms! Hence they say:

LA JOLLA—Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that the virus spike proteins (which behave very differently than those safely encoded by vaccines) also play a key role in the disease itself.

Excuse me? The scientific justification for this claim appears to come from this brief and somewhat confusing statement from the authors themselves:

. . . . . . our data reveals that S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis. It appears that S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM2 upregulation, and ultimately ACE2 destabilization.4 Although these findings need to be confirmed with the SARS-CoV-2 virus in the future study, it seems paradoxical that ACE2 reduction by S protein would decrease the virus infectivity, thereby protecting endothelium. However, a dysregulated renin-angiotensin system due to ACE2 reduction may exacerbate endothelial dysfunction, leading to endotheliitis. Collectively, our results suggest that the S protein-exerted EC damage overrides the decreased virus infectivity. This conclusion suggests that vaccination-generated antibody and/or exogenous antibody against S protein not only protects the host from SARS-CoV-2 infectivity but also inhibits S protein-imposed endothelial injury.

Does that mealy-mouthed scientific explanation make sense? It doesn’t to me. I’m not an expert admittedly but I can sense there is something amiss here. Especially considering the fact that other scientists have also questioned the wisdom of injecting young, healthy people with a ‘vaccine’ which induces their body cells to manufacture the very spike protein which, in severe cases of Covid – which young, healthy people are at very minimal risk from – causes life-threatening cardiovascular disease. Hence, the authors of the PubMed study cited above say:

Vaccines that introduce the spike protein into our body to elicit virus-neutralizing antibodies are currently being developed. In this article, we note that human host cells sensitively respond to the spike protein to elicit cell signaling. Thus, it is important to be aware that the spike protein produced by the new COVID-19 vaccines may also affect the host cells. We should monitor the long-term consequences of these vaccines carefully, especially when they are administered to otherwise healthy individuals.

But, you know, vaccine passport, idiot selfish refuseniks and all that. They’ve simply got to jab every single person on the planet, including your kids, because ‘nobody’s safe until we’re all safe’, right? With the huge and growing number of documented cardiovascular adverse reactions to the ‘vaccines’ (heart attack, stroke, eye damage, haemorrhaging, blood clots, ‘extremely rare’ cerebral haemorrhaging, heavy periods in women) I think it is a near certainty that the spike proteins raised by the ‘vaccines’ do not behave differently at all from the spike protein of the SARS-CoV-2 virus itself and the only difference is that the ‘vaccine’ spike proteins are causing severe cardiovascular disease in people who would not be at significant risk of severe cardiovascular symptoms from SARS-CoV-2 infection, because their innate immune system would prevent the virus from ever progressing to the point where it was able to enter the blood stream and effectively poison the blood with toxic spikes.


It gets murkier. Robin Monotti on Telegram made a Youtube video about this Salk study which they promply deleted, calling it ‘medical misinformation’. What a surprise! However, what did surprise me is that Salk did not originally claim the ‘vaccine’ spike proteins were safe in their initial press release and they actually changed the wording in the article after Robin had released his video. No conspiracy there then.

Note that since I released this video Salk added the words “safely encoded” in their article in their also newly added description of the vaccine spike protein. VAERS numbers indicate this theoretical description does not correspond to the full and complete reality of the situation. Original Salk text was this: “Scientists have known for a while that SARS-CoV-2’s distinctive “spike” proteins help the virus infect its host by latching on to healthy cells. Now, a major new study shows that they also play a key role in the disease itself”

The video is available here on Brandnewtube:


And on Bitchute:

They really, really, really want you to get jabbed with these ‘vaccines’.