Forget dangerous infertility causing vaccines, Covid-19 is prevented by the humble pineapple (say researchers)

On 16th September of this year, a report by researchers at Nebraska University, let’s call them Radhakrishnan et al, was posted at biorxiv.org suggesting that bromelain, an extract from pineapple used as a run of the mill dietary supplement (as an anti inflammatory medicine*), interfered with the mechanics of the illness that is being called Covid-19 (perhaps also known as SARS), by inhibiting SARS-COV2  (SARS-COV) infection. The results of an experiment by Radhakrishnan et al appears to lead them to understand that bromelain has a detrimental effect on the expression of ACE2, or angiotensin-converting enzyme II.

It is highly likely that for any reader coming newly to this site, the term ACE2 will be devoid of meaning, and this would be testament to the work by all media in the English-speaking world which persists in failing to educate its audience about the single most important piece of data that they could know about Covid-19. It is a failure that is particularly dismal in alternative media, which must reveal itself to be controlled, where it is apparently the case that ACE2 should not be discussed under any circumstance.

On the contrary, the FBEL readership is regularly reminded that Covid-19 is a pneumonia as a complication of pulmonary damage caused by SARS-COV binding to ACE2 at the lung – and it is nothing else. Thus, if the tens of thousands who are said to have died of “Covid-19” in the UK did not suffer this specific illness – and only a tiny percentage might have done – they did not die of Covid-19.

So, it should be obvious to the reader that, for undermining the psychological operation by UK Government involving huge death tallies, and stupefying – most likely invented – infection case rates, as a pretext for imposing an economic blockade on medium and small businesses, their owners and employees, there is not any one thing more important than knowing about ACE2. Indeed, any reader who thinks it acceptable that, nearly a year into the arrant nonsense, alternative media will not touch ACE2 with a barge pole, is a person who needs to locate a sense of outrage, and who needs to aim it at their alternative media provider and elicit an explanation from them, or else continue in a state of delusion, investing their time and treasure in being led by the nose to a place where the people who prey on them want them to go.

That being said, in this episode of the very different and very important work that takes place at this site in which the fact of death by ACE2 (though it be rare) is energetically confronted†, we are going to look at a small number of research studies that approach the issue of preventing Covid-19 by what might be called an alternative approach – certainly alternative to the vaccine blunt instrument, which is in fact, in the case of Covid-19, really quite irrelevant.

And indeed, at this time, of course, when the Medicines and Healthcare products Regulatory Agency (MHRA) approved the use in Britain of the vaccine by Pfizer and BinNTech, and did it only two weeks after the vaccine’s efficacy trial was declared done (170 people out of 41,135 got sick with something being called “Covid-19”), it becomes urgent to undermine a public notion that would be formed by government propaganda that there is a necessity for a vaccine, and do it in more ways than one.

The reader may well have heard that Drs Wodarg (the lung specialist and former head of the German public health department) and Yeadon (the ex-Pfizer head of respiratory research) have made a request of the EMA (European Medicines Agency), the “agency of the European Union in charge of the evaluation and supervision of medicinal products” – as the official profile has it – to suspend immediately all SARS-CoV2 vaccine studies, and in particular the BioNtech/Pfizer study.

Of course, this is a door that would be being shut in the UK after the horse has not only bolted, but has galloped a number of country miles down a winding lane. In any case, one of the most serious objections to the Pfizer vaccine is that it could cause infertility, and in quite the pernicious way, as a German, English-language news site details:

The vaccinations are expected to produce antibodies against spike proteins of SARS-CoV-2. However, spike proteins also contain syncytin-homologous proteins, which are essential for the formation of the placenta in mammals such as humans. It must be absolutely ruled out that a vaccine against SARS-CoV-2 could trigger an immune reaction against syncytin-1, as otherwise infertility of indefinite duration could result in vaccinated women.

Confirming that the concern of the two doctors is well founded, the actual information for UK healthcare professionals as published by the government’s assets publishing service states the following (link – pdf):

For women of childbearing age, pregnancy should be excluded before vaccination. In addition, women of childbearing age should be advised to avoid pregnancy for at least 2 months after their second dose…

It is unknown whether COVID-19 mRNA Vaccine BNT162b2 has an impact on fertility.

Clearly the advice reflects the concern of the doctors Wodarg and  Yeadon that the vaccine will affect the development of a foetus.  And as a matter of fact, if there is not data on the impact that the Pfizer vaccine has on fertility so that, as the two doctors say, it could persist if and when created for an indefinite period, the advice of a two months  intermission between pregnancy and a second dose of the vaccine is surely mere guesswork. In fact, the author reads the first sentence in the above extract as if it is saying, women for whom having a baby is possible should not take the vaccine. Little wonder, then,  it is not, at the moment, being targeted at members of the general public who are younger than 50 years old (in fact, it is octogenarians and their seniors who are being lined up to be the first victims). Incidentally, such was the evident worry had by UK Government about a refusal by NHS staff – lots of whom will be women being capable of bringing a baby to term – to be amongst the first to be given the vaccine, that plans were changed, not long after the approval by the MHRA, to remove the requirement that health service personnel be vaccinated in the initial roll out.

Of course, while there has been coverage at FBEL of the risk, in terms of damage to the nervous system, in taking a “Covid-19 vaccine”‡, the absolute carnage that the Pfizer vaccine potentially unleashes was a thing unimagined. The ultimate irony, of course, on top of the usual fundamental flaw of a vaccine where the target virus₸, through mutation, almost certainly will not be the same as the one introduced by the injection, is that the Pfizer vaccine is redundant because it isn’t meant to prevent lethal cases of Covid-19 (see The Pfizer Vaccine’s Meaningless 90% Effectiveness, And The Circus Surrounding It – link). This would make sense, given that it is completely unrelated to the prevention of real Covid-19 (hence the use of the quotation marks, thusly: “Covid-19 vaccine”). And in the end, when one is seriously looking for a preventative cure for the illness that is Covid-19, and not taking part in a propaganda freak show, as we shall see, a vaccine should be understood not to be as effective as a medicine that acts to prevent or inhibit the essential mechanical interaction at the root of the disease: a medicine that prevents SARS-COV from binding with ACE2.

That there is a search for such a medicine, as already stated, is the subject of this article. Now, it must be pointed out, the author would argue that a new medicine would in fact not be required, and that the cure for Covid-19 is the cessation of the creation of high ACE2 levels through the intake of prescription drugs for hypertension and related conditions; i.e. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). (See, Is “Covid-19” An NHS Prescribed Drug-Induced Pneumonia (Amongst Other Things)? – link).

As intuitive as this is, it is apparently a contentious view – as big pharma and the British health industry (with the NHS at its coalface), with lots of money at stake, acts to quash the formation of a bad reputation – even if the study by Radhakrishnan et al talks in terms of a bromelain treatment diminishing the expression of ACE-2; in other words, reducing the level of expression. (An article defending the accusation that Covid-19 is caused by prescription drugs for hypertension has been long in the offing; the delay is to allow for the accruing of relevant studies, or not, that argue for and against the hypothesis).

In any case, what will now follow will be the reproduction of the abstracts, or the introductory parts of reports on three studies that suggest a cure for Covid-19 by interfering with the capability of SARS-COV to bind with ACE2. There will be little further comment from the author of this article; the point is to let the reader see that these studies exist, and that there is a branch of research that undermines the claimed necessity of a vaccine, and again, as has been the custom hereabouts, to show that SARS-COV to ACE2 binding is acknowledged by serious people, thus the fact that controlled media doesn’t mention it has no bearing on it being a reality.

The nature of the fundamental flaw of the “Covid-19 vaccine”  is echoed in the introduction to a report on a study on the use of using a decoy for ACE2 by a group of researchers we’ll call Linsky et al (source):

To infect cells within the respiratory tract, the Spike (S) protein on the surface of SARS-CoV-2 must bind to a receptor on human cells called angiotensin converting enzyme 2 (ACE2). The receptor binding domains (RBDs) are the section of the S protein which binds to hACE2. Disrupting this interaction has become the focus of a lot of research, as it would prevent infection; however, when neutralising antibodies have been developed to target the S protein, it has been shown to evade them by mutating.

The piece then continues…

To address this issue, Thomas Linsky and colleagues created a computational protein design strategy to enable the development of therapeutics that may be more resistant to SARS-CoV-2 mutational escape.

In their study published in Science, the team describe the design, validation and optimisation of stable hACE2 protein decoys which mimic the protein receptor interface to which SARS-CoV-2 binds.

They developed roughly 35,000 computational decoys and took the top-ranking ones into further testing. From these experiments they identified CTC-445.2 as the best decoy. According to the study, CTC-445.2 binds with low nanomolar affinity and high specificity to the RBD of the S protein. Using cryogenic electron microscopy (cryo-EM) they observed that CTC-445.2 also simultaneously bind to all three RBDs…

The team concluded that because the decoy replicates the S protein target interface, it is intrinsically resilient to viral mutational escape.

Hopefully, it is clear to the reader that the researchers in this case were modelling how a decoy could lure SARS-COV from ACE2. It must be pointed out the RBD that is mentioned is a complex including the bit of SARS-COV that hooks onto ACE2 – as explained, if not entire satisfactorily, in the FBEL article, More On SARS-COV-ACE2 Binding & “True” Covid-19 That Discredits UK Government’s Pretext For Creating Economic Disaster. It should also be pointed out that the researchers don’t necessarily need to be modelling with a representation of isolated SARS-COV2 (which doesn’t exist), and hopefully the reason for saying this will also be made clear if the reader follows the link.

In the following, from a paper published at the PNAS website (PNAS standing for Proceedings of the National Academy of Sciences of the United States of America ), the researchers have designed what they call ACE2 receptor traps to capture SARS-COV and prevent the real harmful binding. The reader is asked to notice the sentence,“engineered ACE2 receptor traps offer a promising route to fighting infections by SARS-CoV-2 and other ACE2-using coronaviruses”, because this reminds that SARS-COV2 is essentially SARS-COV until scientists can prove otherwise. (Source [paragraphing for ease of reading]).

An essential mechanism for severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection begins with the viral spike protein binding to the human receptor protein angiotensin-converting enzyme II (ACE2). Here, we describe a stepwise engineering approach to generate a set of affinity optimized, enzymatically inactivated ACE2 variants that potently block SARS-CoV-2 infection of cells.

These optimized receptor traps tightly bind the receptor binding domain (RBD) of the viral spike protein and prevent entry into host cells. We first computationally designed the ACE2–RBD interface using a two-stage flexible protein backbone design process that improved affinity for the RBD by up to 12-fold. These designed receptor variants were affinity matured an additional 14-fold by random mutagenesis and selection using yeast surface display. The highest-affinity variant contained seven amino acid changes and bound to the RBD 170-fold more tightly than wild-type ACE2.

With the addition of the natural ACE2 collectrin domain and fusion to a human immunoglobulin crystallizable fragment (Fc) domain for increased stabilization and avidity, the most optimal ACE2 receptor traps neutralized SARS-CoV-2–pseudotyped lentivirus and authentic SARS-CoV-2 virus with half-maximal inhibitory concentrations (IC50s) in the 10- to 100-ng/mL range.

Engineered ACE2 receptor traps offer a promising route to fighting infections by SARS-CoV-2 and other ACE2-using coronaviruses, with the key advantage that viral resistance would also likely impair viral entry. Moreover, such traps can be predesigned for viruses with known entry receptors for faster therapeutic response without the need for neutralizing antibodies isolated from convalescent patients.

The final research is the one that supplies the material which inspired the title of this article; no further introduction is required. (Source [again, paragraphing for ease of reading]):

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The initial interaction between Transmembrane Serine Protease 2 (TMPRSS2) primed SARS-CoV-2 spike (S) protein and host cell receptor angiotensin-converting enzyme 2 (ACE-2) is a pre-requisite step for this novel coronavirus pathogenesis. Here, we expressed a GFP-tagged SARS-CoV-2 S-Ectodomain in Tni insect cells. That contained sialic acid-enriched N- and O-glycans.

Surface resonance plasmon (SPR) and Luminex assay showed that the purified S-Ectodomain binding to human ACE-2 and immunoreactivity with COVID-19 positive samples. We demonstrate that bromelain (isolated from pineapple stem and used as a dietary supplement) treatment diminishes the expression of ACE-2 and TMPRSS2 in VeroE6 cells and dramatically lowers the expression of S-Ectodomain. Importantly, bromelain treatment reduced the interaction between S-Ectodomain and VeroE6 cells.

Most importantly, bromelain treatment significantly diminished the SARS-CoV-2 infection in VeroE6 cells. Altogether, our results suggest that bromelain or bromelain rich pineapple stem may be used as an antiviral against COVID-19.

* Perhaps it should be mentioned, in the author’s household, bromelain is credited with curing lateral epicondylitis, otherwise known as tennis elbow.

† Here for instance:

SARS-COV To ACE2 Binding And The Dangerous Covid-19 Truth – (link)

‡ Here for instance:

The Oxford-AstraZeneca Trial Illness: One That Only Appears To Have Been Caused By The Vaccine? – (link)

₸ For the sake of precision, the Pfizer vaccine, as a messenger RNA (mRNA) vaccine,  doesn’t use a viral sample, but instead a substance that is exploiting the genetic information of a virus. Expect a follow up to this in a further article, but suffice to say, like AstraZeneca’s chimp cold based vaccine, this solves the problem of SARS-COV2 never having been isolated.