Published On: Thu, Apr 2nd, 2020

More on SARS-COV-ACE2 binding & “true” Covid-19 that discredits UK Government’s pretext for creating economic disaster

Recently, here at FBEL, there was a presentation of the very plausible theory that “Covid-19”, in what we might start to call its truest sense, is caused by coronavirus interacting with Angiotensin-Converting Enzyme 2 (ACE2) receptors expressed in the lungs. It was further posited that a prevalence of ACE2 was a side effect of treatment with ACE inhibitors (ACEI), and angiotensin receptor blockers (ARBs) for hypertension.

Now we look at further evidence that reinforces the fact of the manner of lung infection proposed in the theory, and how ACEIs and ARBs appear to be being used expressly to promote ACE2s for what is limitedly understood to be medicinal qualities; in other words, the ACE2s are not intended to be side effects, but a factor in the treatment. As such, an environment for a limited amount of success by a coronavirus that attacks the lungs has been deliberately created by the medical establishment.

In this article, we will also briefly examine how the Chinese, in their experience of what at first was an unexplained pneumonia, showed definite signs of becoming certain of ACE2 as a factor, and their resort to CT scans was possibly an indicator of this. In any case, the diagnoses by PCR test of a patient being coronavirus harbouring was by no means indicative of capability to develop the particular disease. However, with these details not appreciated (and they have not been in the UK), there cannot be the remotest idea about the very particular circumstances that appear to need to be extant in a host. Indeed, the permutations are such that it should be highly unlikely – to impossible – for a remotely healthy person who has been diagnosed as carrying the target coronavirus to be capable of developing “Covid-19” from it. In conclusion, the Imperial College statisticians, who are in the first instance responsible for the economically disastrous lockdown in the UK by their modelling and predictions for the spread of “Covid-19”, would have been clueless. As such, the Imperial College modelling is grossly, and indeed criminally erroneous and irresponsible.

An article published in Science on 27th March, 2020, describes the research by a team of Chinese scientists, who we will call Yan et al, who have imaged what they call a RBD-ACE2-B0AT1 complex with cryo–electron microscopy. Simply put, they have visualised the binding of a coronavirus to ACE2. Now, it should be pointed out that the team have not seen a SARS-COV-2 entity, which is the supposed cause of Covid-19. Instead, they obtained, from another laboratory, the component part that does the binding. As such, for those who remain sceptical that SARS-COV-2 is different from SARS-COV, there is no revelation here that could force a change of mind.

SARS-COV and SARS-COV-2 appear to be fundamentally architecturally the same; SARS-COV being Severe Acute Respiratory Syndrome coronavirus (the name suggests the effect) that emerged from Guangdong province of China in November of 2002 – or so the story goes. The important thing to grasp about this coronavirus (and this feature is universal to all types) is the surface spike glycoprotein, or S protein. In SARS-COV, this cleaves in two in the process of fusing to another cell; the subparts are called S1 and S2, with the former being the one we need to be interested in. “S1”, explains Yan et al, “contains the receptor binding domain (RBD), which directly binds to the peptidase domain (PD) of angiotensin-converting enzyme 2 (ACE2)”. Now, the reason that there has been a descent into a little more complexity than is desirable is because it needs to be explained that the Chinese research team only had the RBD of SARS-COV-2. Moreover, the reader needs to be introduced to a thing called B0AT1, which is a chaperone protein to ACE2, and appears to have an influence over the PD – although “it is unclear how ACE2 interacts with B0AT1”.

Yan et al appear to imply that the balance of B0AT1 and ACE2 has an effect on the success of SARS-COV to bind to the latter; this might have a bearing on why the coronavirus is problematic in the lungs, and not in other organs where there is a greater expression of B0AT1 (because ACE2 is not only present in the lungs, but the heart, kidneys, and intestine too). What this provides for us is an introduction into an idea that will form a motif for this article, to wit: balance in the terrain is the key factor in health, with illness occurring where there is imbalance.

Amongst the many things we can learn from the Yan et al briefing is the apparent Chinese confidence in a fact of the genesis of Covid-19, and the possession of knowledge for a pathway to a cure; in other words, ACE2 is made the unambiguous culprit:

Scientists are racing to learn the secrets of severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2), which is the cause of the pandemic disease COVID-19. The first step in viral entry is the binding of the viral trimeric spike protein to the human receptor angiotensin-converting enzyme 2 (ACE2)… The structures provide a basis for the development of therapeutics targeting this crucial interaction.

Indeed, in January of this year, the British Medical Journal (BMJ 2020;368:m406) published a discussion confirming the existence of the knowledge in China of ACE2 as a crucial component in the illness:

Yushun Wan, Jian Shang et al have analysed the potential receptor usage by 2019- nCoV based on the knowledge on sequencing of SARS- CoV. They have found that the sequence of 2019 nCoV receptor binding motif that directly contacts ACE2 (receptor Angiotensin converting enzyme 2) is similar to that of SARS–CoV & suggest that 2019-nCoV (Wuhan) uses ACE2 as its receptor. Their structural analysis predicted that the Wuhan Corona Virus uses ACE2 as its host receptor. They have further stated that a single mutation significantly enhances the ability of nCoV (Wuhan) to bind with human ACE2.

With this understood, it might explain why the Chinese were using CT scans in diagnosis of Covid-19. While the fact that a virus or coronavirus being responsible for a disease could not be ascertained this way, what was evidently being searched for was the signs of the symptoms of the binding as might be expected. Again, one could question how certain doctors could be in the notion that they were seeing a mass of RBD-ACE2 binding on the lung, but it’s one to which there is no answer to, here at the moment.

To this point, then, the reader should have ascertained that the Chinese appreciate that coronavirus-S binding with ACE2 in the lung is a real phenomena, and had been taking it into consideration as they were getting to grips with their outbreak of respiratory related ailment. Attributing an underlying cause of Covid-19 to the promotion of ACE2 by usage of ACEI and ARB is another step to make, and it’s not clear if the Chinese have done this (in fact the author has no information about levels of usage of ACEI and ARB in China) – nor indeed if Chinese pharmaceutical companies would tolerate the information being expressed.

However, the proposal has been made by scientists in the west, who even then might not be understanding that a decision might have been taken by those who create as broad a market for drugs as possible to promote ACE2 in patients as therapy: in other words, it is not just a side effect.

It might come as a surprise to the reader that ACE2 is a relatively new discovery. How and where it had been hiding is beyond the ken of the author, and the scope of this work, but nevertheless it is only in the last decade that it has been found. A reasonable guess to be had about the reason for its invisibility, however, is that it has been obscured. The levels of ACE in a body is 200 times higher than ACE2, this according to a paper published by the National Center for Biotechnology Information (NCBI) in 2013, Angiotensin-Converting Enzyme 2 as a Therapeutic Target for Heart Failure. This, it is suggested to the reader, again begins to suggest that the problem with ACE2 is one of imbalance. For, the said paper informs that “ACE and ACE2 are functionally different enzymes that play opposite actions”. To give examples in non-chemistry terms: “loss of ACE2 enhances the susceptibility to myocardial dysfunction, while enhancing ACE2 action prevents adverse pathological remodeling and slows the progression to [heart failure]”. This is saying that ACE2 is a force for good in a cardioprotective role. Conversely, we know that

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are highly recommended medications for patients with cardiovascular diseases including heart attacks, high blood pressure, diabetes and chronic kidney disease to name a few.

This extract is from the abovementioned previous FBEL article quoting Dr James Diaz, and from it we can understand that repression of ACE is considered to be a force for good in a cardioprotective role. Furthermore, the NCBI paper confirms Diaz’s statement that “patients treated with ACEIs and ARBs will have increased numbers of ACE2 receptors in their lungs”, and does so with the following snippets (for example):

Increased cardiovascular expression of ACE2… levels have been demonstrated with treatment of angiotensin receptor blockers (ARB)…

Interestingly, Ang(1–7) levels [which are ‘produced’ by ACE2] are elevated with treatment of ACE inhibitors and ARB.

Moreover, there is a distinct recognition expressed in the paper that increased ACE2 levels would be a desirable thing:

It is conceivable that ACE2 could also constitute a valuable novel target to complement existing therapeutic strategies for managing [left ventricle (of the heart)] dysfunction. Conditions where ACE inhibition and ARB are partially effective, the adjunctive actions of ACE2 may not only reduce clinical escape but also augment the efficacy of interventions.

To round things up, we could speculate that a conscious decision to create an imbalance of ACE2 as a therapeutic method (and to sell drugs [with, in the UK, the NHS acting as the distributor]) has created an environment where the SARS coronavirus (which was unsuccessful in 2002/3) has encountered a slightly easier terrain to thrive in. Naturally, to begin to confirm the theory, one would need to have a fuller picture of the scale of ACEI and ARB medication usage in the 21st century, and a number of other sketchy details more thoroughly defined. However, if there was any truth to it, people would then be offered an opportunity to see the measures taken by UK Government (because the NHS is a component part) in response to Covid-19 as a reaction to that which was self-inflicted; or, better still, as being a twist of the knife that was already plunged into the body, rather than as a new front in a fundamental war for survival.

As a matter of fact, the RBD-ACE2 binding does not have to be the definitive answer. The central message of this article has been the importance for health of the balance in the body’s terrain. We do not know to what extent the chronic pollution in China (not to mention the unhealthy industrial conditions in northern Italy) has contributed to this in the the cases of Covid-19 in those countries (and has anyone ever conceived of a link to expression levels of B0AT1?). However, because of its complexity, we can be certain that very important considerations about terrain as a denier or an enabler of coronavirus to develop into disease is not accounted for in modelling that has caused the lockdown in the UK.

Moreover, the possibility of a “true” Covid-19, and its dependence on some very particular conditions, will completely undermine the illusory version which causes death (which might explain why the UK Government has launched a campaign calling into question the Chinese account of its Covid-19 experience). This ethereal facsimile would, in reality, manifest as the passing of those who would have succumbed to another disease, or people who were ill and had a pneumonic complication that killed them, or people were exposed to a treatment that killed them (whether they had been healthy or not), or people who had another virus that complicated into a fatality. In all these cases, the word, intended in its most ambiguous sense, “coronavirus”, would have been invoked from the mechanical ritual that is useless PCR testing, and deployed to create death as part of a pandemic that isn’t really happening.

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  1. Robert Hardt says:

    Dear fellow researchers I believe without a doubt did the pre-existing conditions all of them as a matter fact even people that are vaping young people are having these receptors blocked in the body rebounds by making more of them this is the evolution of the bodies immune system therefore you have hundreds maybe even thousands of more sites for the virus to enter into the cell and you are in a replication overcome and caused an auto immune deficiency in eventual cascade of viral infection and inflammation resulting in CYTOKINE storm!

    If you go around the Internet right now you will see that the big farmer boys are blocking all of these sites and recommending the doctors continue to give these medications when they should put a stop immediately and investigate It!, … because we are not as human beings guinea pigs or rats to be experimented on anytime there’s a potential to cause harm or death the pharmaceutical industry needs to get the hell back stick their profits up their butt and start doing what they need to do to make sure that our safety is first in foremost!